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The Roskamp Institute funded by the Veterans Administration to find cellular mechanism implicated in the Gulf War Illnesses

The Veterans Administration announced that by November 2004, veterans who served in the Gulf War between 1990 and 1991 experienced illnesses of unknown etiology which were subsequently categorized as “Gulf War Illnesses”. The Veterans Administration acknowledges a need for systematic scientific identification of the specific molecular mechanisms underlying this disease, from which development of treatments may emerge. The Veterans Administration is particularly dedicated to improving healthcare for veterans who served in the Gulf War.

Michael Mullan MD, PhD (Director of the Roskamp Institute) and Fiona Crawford PhD (Associate Director of the Roskamp Institute) received a three-year grant from this esteemed agency to fund the research on genomics and proteomics analysis of cellular responses to Gulf War agents. Drs. Michael Mullan and Fiona Crawford were previously funded through the Counterdrug Technology Assessment Center (CTAC) to evaluate these advance genomics and proteomics technologies for potential use in identification of biological pathways implicated in neuropsychiatric diseases. Thus, this is a great collaborative union between US government agencies to help find treatments for illnesses that affect our beloved veterans.

This funded proposal will utilize genomics and proteomics technologies among other state-of-the-art resources available at the Roskamp Institute and its affiliated laboratories at the James A. Haley VA Hospital to characterize the cellular responses to biological warfare agents. At the Roskamp Institute, these technologies will be applied to investigate and characterize the in vitro responses to agents such as acetylcholinesterase inhibitors (i.e. pyridostigmine bromide, organophosphate pesticides) and anthrax vaccination. By identifying biological and cellular mechanisms modulated in response to these exposures in the simple in vitro models, the Roskamp Institute scientists will identify initial responses to these agents and then determine if they become pathological with disease progression. This research by the Roskamp Institute will increase our understanding of the underlying mechanisms of these illnesses as well as present targets for potential therapeutic intervention.

The Roskamp Institute is dedicated to exposing the causes of and finding novel treatments for neuropsychiatric, neurodegenerative and addictive disorders. The Roskamp Institute was founded in 1998 by the philanthropic visions of Robert and Diane Roskamp of Sarasota, Florida. In 2003, under the directorship of Dr. Michael Mullan and through the generous support of Mr. and Mrs. Roskamp, the Roskamp Institute was relocated to Sarasota, Florida. The Roskamp Institute, at present, is funded by various US government agencies, such as the National Institute of Aging, the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK), CTAC, the US Department of Defense and the Veterans Administration. Currently, the Roskamp Institute occupies approximately 41,000 sq ft of facility with over 50 brilliant scientists engaged in creative research endeavors to find treatments for neuropsychiatric disorders and clinicians who are dedicated to helping patients and their family members cope with these devastating disorders.

for more information on Alzheimer’s and the Roskamp Institute please visit:

http://www.mullanalzheimer.com

http://www.mullanalzheimer.info

www.rfdn.org

The Roskamp Institute Battles Drug Abuse

A National Survey on drug abuse in America reported in 2004 that about 34 million Americans are currently using or have been exposed to cocaine at some point in their lifetime. Cocaine is highly addictive and affects individuals along with their families. The cost of health care services has risen due to the increasing use of cocaine. Currently, the Roskamp Institute is involved in research to discover a treatment for substance abuse. Dr. Michael Mullan MD, PhD is the director of the Roskamp Institute and has worked vigorously on addiction and has found that addictive disorders have a significant genetic component. These genetic components play a key role in drug abuse.
The Roskamp Institute scientists have previously shown that a genetic change called polymorphism in a gene for an opioid receptor in the brain is a risk factor for alcohol dependency. With this information, the Roskamp Institute researchers then examined the frequencies of this polymorphism carrying genotypes and alleles in numerous groups of individuals addicted to the substance versus individuals with no history of addiction to the substance. These Roskamp Institute scientists found that the mu-opioid receptor’s polymorphism is a genetic risk factor for substance dependence but not to any particular type of drug. Meaning, an individual with this polymorphism is more likely to become addicted to a substance than an individual without it. The Roskamp Institute previously published these findings in the journal Molecular Psychiatry.
Dr. Mullan and Dr. Crawford along with the other researchers at the Roskamp Institute received an award from the Counter drug Technology Assessment Center (CTAC), to continue their work on drug addiction.
Affymetrix is a name of the company which provides the Roskamp Institute with the genetic software that is used by scientists who study genetics (genomics). The Roskamp Institute used genomics technology in order to find the cocaine’s affects on the brain cells known as neuronal cells. The Roskamp Institute scientists continue to research projects which are focused on the inflammatory and immune responses to cocaine. The Roskamp Institute scientists showed that these responses also results from the exposure of the neuronal cells to cocaine and these responses are also time dependant. These findings, originally published in the Journal of Neurochemistry, illustrate that there are biological and physical consequences of cocaine addiction.
The Roskamp Institute researchers are currently working on studies involving oxidative stress in the brain. This oxidative stress can also be caused by excessive use of cocaine and is hypothesized to result in permanent brain damage. With such experiments in progress, the Roskamp Institute is a good candidate for additional government funding and these discoveries will be useful towards the battle against drug abuse in form of treatments.

The Traumatic Brain Injury Program at the Roskamp Institute

Among the soldiers who survive conflicts in Iraq and Afghanistan, the traumatic brain injuries account for a larger proportion of their casualties than in any other US war in recent history. According to the Joint Theater Trauma Registry, established by the U.S. Army Institute of Surgical Research, approximately 22 percent of the injured US soldiers received injuries to the head, face, or neck. A major reason for this high ratio of these injuries is Kevlar body armor and helmets. Although, it successfully protects these soldiers from bullets and shrapnel exposure,Kevlar helmets cannot fully protect theface, head, and neck areas. Additionally, it is also unsuccessful in preventing the closedbrain injuries produced by blasts. Furthermore, among patients evaluated at Walter Reed hospital, closed head injuries outnumber other penetrating injuries (originally published in New England Journal of Medicine).

Most individuals with a mild traumatic brain injury improve entirely within a year,but moderate and severe brain injuries are more complex and have long-term consequences. The Center of disease Control and Prevention estimated that 5.3 million Americans are living with disabilities resulting from traumatic brain injury. Dr. Michael Mullan (Director of the Roskamp Institute) Dr. Fiona Crawford (Associate Director of the Roskamp Institute) and their team of scientists previously demonstrated that apolipoprotein E (APOE) influences traumatic brain injury outcomes. These Roskamp Institute scientists examined 110 participants from the Defense and Veterans’ Head Injury Program to determine a relationship between APOE genotype and memory performance on certain cognitive tests administered to these head injured soldiers. The memory performance was much worse in soldiers who had at least had one APOE epsilon 4 allele compared to those who did not. This Roskamp Institute team also determined that these findings were limited to memory and not other cognitive performances such as executive functioning. Therefore, these data support a specific role for the APOE protein in memory outcome following TBI, and suggest an APOE isoform-specific effect on neuronal repair processes (originally published in the journal Neurology).

Dr. Fiona Crawford received a Merit award from the Veteran’s Administration to further study, using genomics technology, the role of APOE in Traumatic Brain Injury. Dr. Fiona Crawford and her Roskamp Institute team have now completed the experiments showing differences in genomics response among the different mouse models after traumatic brain injury. Recently, Drs. Michael Mullan and Fiona Crawford received a prestigious award of $1.5 million from the Department of Defense which will allow the Roskamp Institute to investigate ApoE and other proteins to find potential peripheral biological markers and novel therapeutic treatments for traumatic brain injury. Florida Senator Bill Nelson recently toured the Roskamp Institute to observe its traumatic brain injury program in support of the soldiers affected by this devastating condition.

The Roskamp Institute is a world-renowned state-of-the-art research and clinical facility located in Sarasota Florida dedicating to finding novel therapeutics for treatment of neuropsychiatric disorder, especially Alzheimer’s disease, traumatic brain injury and substance abuse. The Roskamp Institute is supported by the funding from government agencies such the National Institutes of Health, the Veteran’s Administration and the Department of Defense as well as private donations from the Robert and Diane Roskamp Foundation.

for more information on Alzheimer’s please visit:

http://www.mullanalzheimer.com

http://www.mullanalzheimer.info

www.rfdn.org

Roskamp Institute finds one of the genetic causes for Tourettes syndrome

Tourette syndrome (TS) is a heterogeneous childhood disorder and occurs with a frequency of approximately four to ten per 10,000 in the general population (Mason et al. 1998). The symptoms for Tourette syndrome include multiple motor and one or more vocal tics. These symptoms appear to overlap with other neurobehavioral disorders such as obsessive-compulsive disorder, attention deficit/hyperactivity disorder, mood disorders and learning disorders. The origin of Tourette syndrome is not clearly understood at this time. However, there appears to be presence of a genetic component, evidence for which comes from both family and twin studies. Furthermore, a complex mode of inheritance has been suggested which probably involves several genes with different effect size. Additionally, environmental factors such as prenatal and birth complications may also influence the disease manifestation.
The Roskamp Institute scientists Drs. Michael Mullan (Director of the Roskamp Institute), Fiona Crawford (Associate Director of the Roskamp Institute) and Ghania Ait-ghezala (a senior scientist at the Roskamp Institute) have previously shown that among patients diagnosed with Tourettes syndrome in two unrelated families, there appears to be a breakage and translocation on chromosome 8 (original findings published in the journal Human Genetics). Drs. Fiona Crawford and Ghania Ait-ghezala subsequently received funding from the Tourettes syndrome association to further characterize this chromosomal breakage.
Currently, there is no treatment available for Tourettes syndrome. Although, the symptoms in most individuals improve by the late teens and early 20s, this disorder is generally lifelong and chronic. Studies have also shown that although symptoms such as tics may disappear after the childhood period, it is possible that other psychiatric disorders such as depression, panic attacks, mood swings, and antisocial behaviors persist and cause lifelong impairment in adults. Therefore, a treatment for this disorder is much needed so that a child can actually be disease free throughout his/her life and has a decent chance of living a normal life. The Roskamp Institute is currently engaged in molecular biological research aimed at determining the genes that are disturbed when this chromosomal breakage and translocation occur. Through this novel finding, the scientists at the Roskamp Institute hope to discover a treatment for Tourettes syndrome.
The Roskamp Institute is located in Sarasota Florida and is a not-for-profit stand alone research institute dedicated to finding cures for neuropsychiatric disorders. The Roskamp Institute is currently conducting a clinical trial evaluating safely and efficacy of nilvadipine for the treatment for Alzheimer’s disease (clinical trial being performed in Dublin, Ireland). Furthermore, the Roskamp Institute is conducting various molecular biological studies to find treatment for chronic diseases such as cancer, diabetes, and other neuropsychiatric disorders such as traumatic brain injury, gulf war syndrome, and substance abuse. The Roskamp Institute operates two memory disorder clinics located in Sarasota and Tampa, Florida. These clinics conduct diagnostic assessments for memory disorders and conduct industry and government funded clinical trials in several neurological and neuropsychiatric disorders. The Roskamp institute is currently funded by the National Institutes of Health, the Veteran’s Administration, the Department of Defense and the private donation by the Robert and Diane Roskamp foundation. For more information or the research or clinical trials, please contact us at 94-752-2949.

Sarasota’s Roskamp Institute Welcomes U.S. Senator Bill Nelson

August 21, 2007

Sarasota, Fla. – The Roskamp Institute today welcomed U.S. Senator Bill Nelson to its research facility in Sarasota, Florida, where the Senator toured the laboratories and discussed the various types of research currently being conducted at the Institute.

“We thank Senator Nelson for his interest in our research and for coming to the Institute to tour our lab and view our good work first hand,” said Dr. Michael Mullan, director of the Roskamp Institute. “We are proud of the research our Institute has done and look forward to continuing in our quest to better understand and ultimately cure debilitating diseases of the mind.”

While Senator Nelson’s visit was mainly to discuss with the researchers the current and future research being done in relations to Traumatic Brain Injury, the Roskamp Institute is devoted to understanding the causes of and finding cures for various neuropsychiatric and neurodegenerative disorders and addictions. Specifically, the Institute utilizes a broad range of scientific approaches to understand the causes of and potential therapies for these disorders with an emphasis on Alzheimer’s disease.

“We currently have 45 scientists and 10 clinicians with eight active clinical trials in the field with several more on the horizon,” Dr. Mullan continued. “It is vital that we are persistent in our pursuit to help Florida’s sufferers and their families and we are glad Senator Nelson is here to share in our goal.”

The Roskamp Institute has built its esteemed reputation amongst the research community and has been heralded for its achievements including:

• Being the first Florida-based Alzheimer’s Research Institute (and one of only a handful of Institutes worldwide) to conduct a human clinical trial with a drug discovered by its own research.
• Discovering a new class of drugs that lower the production of the main pathological protein that causes Alzheimer’s disease.
• Applying state of the art technologies (proteomics and genomics) to find early diagnostic markers for Alzheimer’s disease.
• Extensive participation from Florida residents in the Institute’s leading edge Alzheimer’s research program.

for more information on Alzheimer’s please visit:

http://www.mullanalzheimer.com

http://www.mullanalzheimer.info

www.rfdn.org

Dr. Mullan’s Alzheimer Research Offers Invaluable Insights On The Disease

Millions of people across the globe suffer from Alzheimer’s disease. It is estimated (Alzheimer’s Association, 2008) that in every 71 seconds someone from the US develops Alzheimer’s disease, and estimations by mid-century shows that the probability of someone developing Alzheimer’s disease is every 33 seconds. At present, there are approximately 5.2 million Americans in all age groups who suffer from Alzheimer’s disease; and 13% of these patients fall in the age category of 65 years and older. It is calculated that by 2050 the number of Alzheimer’s patients falling in the age category of 65 years and older will increase to a range of over 11 million to 16 million alone (Alzheimer’s Association, 2008). The facts and figures are alarming and bring our focus to the unmet demand for effective therapeutics and new researches for treatments related to Alzheimer’s disease.
Dr. Michael Mullan is an accredited professional from biomedical field. He has extensively researched on the causes and prospective cures of Alzheimer’s disease and other neurodegenerative disorders conditions. Based in Sarasota, Florida, he is reputed Director of Roskamp Institute. He is a highly qualified professional and has dedicated his time to finding cures for neuropsychiatric and neurodegenerative disorders and addictions. Dr. Mullan’s Alzheimer research work has provided invaluable insights on the disease with which many potential cures have been developed and tested. Dr. Mullan’s Alzheimer research indicates that one of the causes directly related to the disease is the excess accumulation of beta-amyloid, a type of protein, present in the brain. It was estimated that the protein is produced in every human but its excess accumulation can result in Alzheimer’s. Besides, Dr. Mullan’s Alzheimer research continuously tests medications and therapeutic treatments to help slow down the accumulation of beta-amyloid and related inflammation in patients.
About Dr Michael Mullan
Dr Michael Mullan has been working in the biomedical field for many years. He is a leading researcher with special expertise in assessment of the earliest cognitive symptoms and stages of Alzheimer’s disease. Mullan’s Alzheimer research works are also published in various articles which help students and researchers for making new discoveries. Find out more about his Alzheimer research works, by browsing through www.rfdn.org or www.mullanalzheimer.com or www.mullanalzheimer.info.

Dr. Mullan’s Alzheimer Research Identified Various Genetic Variations

Based in Sarasota, Florida, The Roskamp Institute is a not-for-profit organization. It has dedicated time to finding cures for several neuropsychiatric disorders with a special emphasis on Alzheimer’s disease (AD). In order to develop therapeutic targets which are specific to Alzheimer’s disease etiology, the scientists engaged in current research at Roskamp Institute focus on dissecting the molecular biological pathways which are associated in Alzheimer’s disease pathogenesis.
Dr. Michael Mullan is the Director of the Roskamp Institute, and along with his team, he discovered the concept of ‘Swedish mutation’, a genetic error which results in overproduction of beta-amyloid by aberrant proteolytic processing of amyloid precursor protein (APP). The concept of Swedish mutation now forms the bases of most mouse model of Alzheimer’s disease. Many tests and findings by the Roskamp Institute resulted in several therapeutic prospects for the treatment of Alzheimer’s disease as well as Cancer.
The Roskamp Institute has contributed greatly by providing research on the treatments of several neuropsychiatric disorders like traumatic brain injury, substance abuse, and Alzheimer, etc. With the guidance and knowledge provided by Dr. Mullan, the institute tested many causes and correlations between Alzheimer’s disease and proteins present in human brain. With Dr. Mullan’s Alzheimer research, several types of genetic variations, which can be the cause of Alzheimer’s, have been identified. It was discovered that the central reason to the disease process is a small protein identified as the ß (beta)-amyloid. Although, this protein is present normally in the human brain, but at times excess or abnormal accumulation can result in Alzheimer’s disease. With Dr. Mullan’s Alzheimer research, the institute tests cutting edge cures, therapeutic treatments and medications to slow down the process of toxic ß-amyloid accumulation.
Dr Mullan’s Alzheimer research proves that Aβ peptide prevents blood vessel growth and eventually inhibits tumor growth in brain. To identify if Aβ has the same effect with short derivatives, he studied various sequences within the Alzheimer’s Aβ peptide which have potential therapeutic relevance in preventing tumor growth. Dr. Mullan’s Alzheimer research work has contributed exceptionally to the field to help understand the disease and find its cures. Find out more about his Alzheimer research works, by browsing through www.rfdn.org or www.mullanalzheimer.com or www.mullanalzheimer.info.

Family History of Alzheimer's disease - what does it mean?

Frequently in the Roskamp institute Memory Clinic we are asked what a family history of Alzheimer’s disease means for the children and other blood relatives of sufferers. Although this question is always handled on an individual basis there are some general guidelines that can be offered to access risk for the disease to children and other family members related to a sufferer. Naturally, family members who perceive they are at risk for developing the disease themselves may suffer from a great degree of anxiety it is therefore important to ask the staff at the Roskamp Institute what the individual risk is for developing the disease. In general the genetic risk for Alzheimer’s disease can be divided into two categories; early onset familial disease which is highly genetic and occurs in families which may have onsets of the disease in the 40s,50s or 60s; late onset disease which is frequently familial but where the disease onsets in the seventh decade onwards. We shall consider these two scenarios separately.

Early onset Alzheimer’s disease.

The term “early onset Alzheimer’s” is frequently misunderstood or used in a confusing way. What we generally mean by early onset Alzheimer’s is Alzheimer’s that onsets before the age to 60 years. This is in contrast to the term early onset as referencing the early stage of the disease. This is a confusing way to use the term and is discouraged. Early stage disease is a better term to describe the early phases of the disease. Early onset familial disease occurs in families that are affected in multiple generations by mutations in genes that can trigger the disease. Families of early onset disease thankfully are very rare but they have provided great insight into the disease process probably in all cases of the disease (early and late onset). Sadly, frequently in these families the disease is inherited in what is known as an autosomal dominant fashion. Autosomal dominant inheritance means that 50% of the offspring of each generation on average are impacted by the disease. Some generations may be very fortunate and although they may be at risk for inheriting the diseased gene from one or the other parent none of the siblings in a sibship may be affected. On the contrary sibships can be very unlucky in which case more than 50% are impacted with the disease. For each child of an affected parent there is a 50% chance of inheriting the disease and this chance is not influenced by whether other siblings have already inherited the disease or not.

Unfortunately the inheritance of these rare genetic variance means that individuals at risk are highly likely to develop the disease if they live long enough. One of the important characteristics of these familial mutations is that the disease tends to onset around approximately the same time of life. Thus if a family has a mean (average) age of onset of 52 and one inherits one of these rare generic errors then one is unlikely to live to 60 without developing signs or symptoms of the disease. By contrast if one does not carry the mutation then there is no more risk for the disease than the general population.

Again it is most important to emphasize that such families are extremely rare and early onset Alzheimer’s is not the most likely reason for patients or their families to visit the Roskamp Institute Clinic. In fact, approximately 1% or less of cases of Alzheimer’s Disease have what can be described as early onset disease. In the past, individuals who come from such families have sought genetic counseling including genetic testing for these genetic errors. It is relatively straightforward to detect such errors but clearly the genetic information is highly sensitive. Family members should therefore think very carefully before seeking such information however initially finding out more about early onset disease is a recommended step.

Clinicians at the Roskamp Institute are happy to discuss early onset disease with patients and their families as they wish. Finally it should be noted that many cases of early onset disease occur without a family history. Thus individuals can manifest the disease before the age of 60 but have no other known family members either in the prior generations or in subsequent generations that develop the disease the cause of early onset Alzheimer’s that is not familial is not well understood but importantly there is no risk to subsequent family members for development of the disease.

Late onset (common) Alzheimer’s disease. Much more commonly patients and their families come to the clinic at the Roskamp Institute and seek advice on the inheritance of Alzheimer’s when one or more members of the family has late onset disease. This is defined as disease which onsets over the age of 60 and this is by far in a way the most common cause of the disease. It is estimated that approximately 4 million Americans presently either have the disease or are in the early or pre clinical stages - most of these cases are late onset Alzheimer’s Disease. The predicted numbers for future disease prevalence are very high. For instance it is estimated that by mid century there could be as many as two hundred million individuals afflicted with the disease.

Most late onset Alzheimer’s disease does not exhibit a clear autosomal dominant pattern meaning that the risk to offspring of individuals suffering with the disease is usually considerably less than 50%. Certain genetic risk factors for late onset disease have been identified - the most important of which is apolipoprotein E (APOE). There are 3 common forms of APOE: E2, E3 and E4. The discovery by Allen Roses and his colleagues at Duke University showed that Alzheimer’s disease sufferers were much more likely to carry one or two copies of the E4 allele (genetic form) of APOE than the normal population. Carrying one copy of APOE 4 increases ones risk for the disease by approximately three times and carrying two copies can increase the risk for the disease by up to fifteen times compared to individuals who do not carry an APOE 4 allele.

Many family members express interest in being genetically tested for their risk for the disease. Such tests are commercially available but most centers discourage the use of testing prior to symptoms because many individuals who carry an APOE 4 allele do not necessarily develop the disease at least until late old age. Conversely it’s very possible to develop Alzheimer’s disease without carrying an APOE 4 allele. Therefore on an individual basis the test is not overly helpful in specifying who may or may not develop the disease. However on a group basis APOE genetic testing is very helpful to give an average estimate of the numbers of individuals who will subsequently develop Alzheimer’s.

It is anticipated that as better treatments are available for Alzheimer’s disease there will be greater interest in genetic testing. For instance it is expected that as treatments are used earlier and earlier in the stages of the disease that individuals in the very early stage or maybe with no symptoms at all might seek medical treatment once such treatment has been established as effective in stopping the rate of progression or disease onset.

Despite the fact that genetic testing is not used frequently in clinical practice it is a tremendous tool in assisting researchers in understanding when and why the diseases develops and in planning clinical trials to take into account who is most likely to develop the disease. Already there is evidence from several clinical trials that individuals that carry the APOE 4 allele may be more refractory to certain treatments. As drug development progresses it will be important to develop medications that are able to tackle the severest form of the disease i.e. those patients who are carrying and APOE 4 allele.

Summary: The two types of familial Alzheimer’s disease differ in the risk for offspring of developing the disease. The early onset cases as noted have children that are highly at risk for developing the disease if there is a family history. By contrast late onset disease or low clustering in families is much less genetically predisposed. In both cases genetic tests are available but are generally discouraged particularly for late onset disease. Roskamp Institute researchers and clinicians are well versed in the genetic aspects of the disease and can advise on an individual or family basis as required.

The Roskamp Institute is a not-for-profit research Institute located in Sarasota and Tampa, Florida, that is dedicated to understanding the causes of, and finding cures for, neuropsychiatric and neurodegenerative disorders and addictions with an emphasis on Alzheimer’s disease. The Institute’s Memory Clinics also offer comprehensive cognitive and medical assessment toward differential diagnosis of Alzheimer’s disease and offers treatments and disease management options once the diagnostic evaluation is complete

By Dr. Michael Mullan, Director of Alzheimer Research Institute, The Roskamp Institute

for more information on Alzheimer’s please visit:

http://www.mullanalzheimer.com

http://www.mullanalzheimer.info

ß-amyloid exchage in the blood-brain barrier

Why work with Alzheimer's disease patients?

Walking into the Memory Disorder Clinic at the Roskamp Institute one might ask “Why work with Alzheimer’s patients and their families?” The answers are manyfold. One of the most rewarding aspects of working with Alzheimer’s patients is that they are most commonly our oldest citizens who have 60, 70 or 80 years of life experience behind them many of them have served their country in one form or another - frequently in the military but often times in businesses working for others or their own companies. Many of those serving in the armed forces have captivating stories. One visitor to the clinic had parachuted into three war zones Normandy, the “boot” of Italy, and Germany. Remembering this tale this gentleman was most afraid of being shot by the Russians! Of course being able to recall these old memories is not unusual for Alzheimer disease suffers. In fact the tendency to reminisce sometimes becomes a prominent feature of the disorder. Most caregivers are initially concerned by another aspect of the disorder namely the forgetfulness for recently acquired or presented information. Such things as recent visits recent phone calls or recent conversations and events may not be remembered either in part or in full. This distressing symptom interferes with social activities and is a progressive aspect of the disease. Therefore one of the most rewarding aspect of working with Alzheimer’s sufferers and their families is being able to convey to them the several treatment options that are available. This includes, as well as those drugs approved by the FDA, new and experimental treatments including those that are being developed by the Roskamp Institute itself.

Providing hope for patients and their families is a critical part of interfacing with them. In addition helping families to come to terms with a disorder that can impact many aspects of their love ones’ lives (including social interactions, pastimes and sports, financial transactions and medical legal issues) enables families to make the necessary adjustments to deal with the condition. Naturally a particularly satisfying interaction can occur when certain elements of a patient’s health can be altered to improve the outcome once a diagnosis of Alzheimer’s has been made. For instance we know that cardio-vascular health interacts critically with Alzheimer’s disease and aversion of cerebrovascular events (such as small strokes or transient ischemic attacks) has a highly beneficial effect on the outcome of Alzheimer’s patients. In addition other conditions such as diabetes or thyroid disease can interact negatively with the disease. These and many other treatable causes of cognitive dysfunction appear at the Roskamp Memory Clinic and are regularly amenable to intervention. Sometimes previous diagnoses are found to be incorrect and memory loss may be completely reversible. For instance people suffering from normal pressure hydrocephalus have a condition that is completely amenable to surgical correction.

Another gratifying aspect of working with Alzheimer’s patients is being able to give their families and loved ones a clear indication of what the treatment options are and what the outcomes are likely to be. In addition family members are often concerned about their own risk for developing the disease it now being common knowledge that the disease has a familial aspect.

All in all there is much to recommend a profession working and caring for Alzheimer’s patients. Our elderly are frequently amongst our most valued citizens who have contributed to the prosperity and safety of subsequent generations. Continuing to work for their immediate care and finding new treatments to improve their long term prognosis are the premier interests of the Roskamp Institute’s researchers, physicians and clinicians.

Alzheimer's disease drug developed at Roskamp Institute approved for key clinical trial funding in Europe

Nilvadipine, an Alzheimer’s drug developed at the Roskamp Institute in Sarasota announced earlier this year was selected for funding or a large-scale European clinical trial. An international research consortium led by Trinity College Dublin (Ireland) announced more than 500 patients will participate in the multicenter Phase III clinical trial designed to study the effectiveness of Nilvadipine.
Michael Mullan, M.D., Ph.D., Roskamp Institute director who, with associate director Fiona Crawford, Ph.D and lead scientist Daniel Paris, Ph.D., led the research team that developed the drug. Mullan said, “We need many more medicines to move forward into advanced clinical trials in the fight against Alzheimer’s Disease and we are pleased the Roskamp institute has played such a major role in the development of this drug.” Before a drug can move into clinical practice, Phase III is usually the last step in the regulatory process.
The clinical trials will take place in Europe, where Brian Lawlor, M.D., Connolly Norman Professor of Old Age Psychiatry at Trinity College Dublin, Ireland, will be principal investigator and coordinator. The study will be funded by the European Commission Seventh Framework Programme and more than 20 European clinical sites will participate. Nilvadipine is already approved for the use in mild cases of hypertension (high blood pressure) and Mullan says, “The process can move more quickly in Europe, and the study findings may help accelerate the process with the U.S food and Drug Administration (FDA).
Mullan and Crawford have been studying Alzheimer’s disease for more than 20 years, moving from the UK to Florida in 1991 and to Sarasota in 2003 to establish the Roskamp Institute. “Some of our recent studies have involved Sarasota area residents, who have contributed to our understanding of Alzheimer’s disease and helped move the development process forward,” said Crawford. Now, the Roskamp Institute will provide research support for the Phase III clinical trial, such as assessing genetic and other markers for Alzheimer’s disease in study participants.
For more information on Alzheimer’s Disease please visit www.mullanalzheimer.com
Or http://mullanalzheimer.info
Or www.rfdn.org

Roskamp institute studies may lead to better diagnosis

Researchers at the Roskamp Institute have new studies that could lead to better diagnosis and eventual treatment for U.S. military personnel as well as other patients with TBI, commonly known as traumatic brain injuries.
Fiona Crawford, Ph.D., associate director of the Institute, a leading research facility for Alzheimer’s disease and other neurological disorders says, “We have found that there are changes in blood proteins that occur after a head injury, and that these are dependent on the severity of the injury, the time since the injury and genetic factors influencing outcomes after head injury.” Crawford’s research indicates that TBI can affect cellular mechanisms in the brain long after the original trauma, and that blood biomarkers reflect these ongoing processes. She also stated, “Translating these finding from the laboratory to human patients may help clinicians determine the extent of the brain injury, how long ago the injury occurred and the patient’s prognosis for a favorable or a poor outcome.”
Traumatic brain injury has multiple consequences at the cellular level and so molecular changes can persist for weeks and months after the initial brain swelling and other immediate issues have resolved. Crawford says, “Identifying blood biomarkers of mild TBI would improve medical management by enabling us to identify patients who need treatment or intervention, even if they do not have obvious signs of a brain injury.” The U.S. Department of Defense, and the Veterans Administration supports all of Crawford’s work because it could lead to better diagnosis of military personnel with mild brain injuries and better long-term care of our veterans.
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Dr. Mullan’s Alzheimer Research Involved Studying Brain Proteins

The Roskamp Institute has surfaced as a leading and reputable non-for-profit biomedical research organization. It has successfully experimented to find cures for several neurodegenerative disorders and conditions like Alzheimer’s disease. Through the clinical trials division and outpatient clinic, at the institute, thousands of Alzheimer’s patients get superior services and therapeutic treatments. Dr. Michael Mullan is the Director of Roskamp Institute. Dr. Mullan is an experienced and a competent individual. His research efforts led to the identification of Swiss Mutation.
Along with Dr. Mullan, the institute has helped in contributing to provide insights on the treatments of neuropsychiatric disorders such as Alzheimer, traumatic brain injury, substance abuse, etc. through unparalleled research. Under the supervision and guidance of Dr. Michael Mullan, several causes and cures related to Alzheimer’s disease have been found. Dr. Mullan’s Alzheimer research identified various types of genetic variations which may be the cause of predispose humans to this disease. His research and study identified that the central reason to the disease process is a small protein known as ß (beta)-amyloid. The excess and abnormal accumulation of ß-amyloid in the brain results in Alzheimer’s disease. With Dr. Mullan’s Alzheimer research, cutting edge cures, medications, and therapeutic treatments are tested and developed to help slow down the process of ß-amyloid’s toxic accumulation.
As per the research on Dr Mullan’s Alzheimer, Aβ peptide is responsible for preventing blood vessel growth and inhibiting tumor growth. He studied several particular sequences within the Alzheimer’s Aβ peptide to identify if Aβ can have the same effect with short derivatives as well. The research proved that the peptide has potential therapeutic relevance to prevent the growth of tumor. The research involved conducting clinical trials which are specifically conducted to developing superior treatments for neurodegenerative diseases. In order to understand the diseases and finding its causes and prevention, Dr. Mullan’s Alzheimer research work has contributed extraordinarily in the field. Furthermore, with his constant efforts and guidance, the Roskamp Institute was also able to carry out research in neuropsychiatric disorders such as Traumatic Brain Research, Gulf War Illness, and Alzheimer’s. Find out more about his Alzheimer research works, by browsing through www.rfdn.org or www.mullanalzheimer.com or www.mullanalzheimer.info.

The Direct Causes Related To The Disease

Alzheimer’s disease affects patients over 65 years of age and is classified as a type of dementia. However, the less prevalent early-onset Alzheimer’s can also occur earlier than 65 years of age as shown by several researches. As per the 2006 statistics, there were 26.6 million patients of Alzheimer’s and it is estimated that the disease will affect 1 in 85 people globally by 2050. Presently, there are no cures available for the disease and it is estimated to get worse with age gradually leading to death. Alzheimer’s is calculated to affect a person’s memory, affects the ability to learn and also types of behavioral changes.
Dr. Michael Mullan is a highly accredited biomedical professional and has contributed vastly to the field of research on neurodegenerative disorders conditions such as Alzheimer’s disease. He is chaired as the Director at Roskamp Institute. He is based in Sarasota, Florida, and is exceptionally qualified in finding cures for neuropsychiatric and neurodegenerative disorders and addictions. The Roskamp Institute utilizes superior scientific approaches along with Dr. Mullan to understand the root causes and potential therapies of disorders such as Alzheimer’s disease. Aside researching on Alzheimer’s, the institute has successfully studied other illnesses and disorders such as Gulf War Illness, Brain Research, etc.
With Dr. Mullan’s Alzheimer research, science has come to a better understanding of the disease and of developing its prospective cures. Dr. Mullan’s Alzheimer research proves that one of the direct causes related to the disease is the excess accumulation of beta-amyloid which is a type of protein in the brain. It is noticed that the protein is produced in every human, but its excess accumulation can result in Alzheimer’s. Along with the team, Dr. Mullan’s Alzheimer research has tested many medications and therapeutic treatments to help slowing down the accumulation of beta-amyloid and associated inflammation.
About Dr Michael Mullan
Dr Michael Mullan has been working in the biomedical field for many years. He is a leading researcher with special expertise in assessment of the earliest cognitive symptoms and stages of Alzheimer’s disease. Mullan’s Alzheimer research works are also published in various articles which help students and researchers for making new discoveries. Find out more about his Alzheimer research works, by browsing through www.rfdn.org or www.mullanalzheimer.com or www.mullanalzheimer.info.

Potent anti-angiogenic motifs within the Alzheimer beta-amyloid peptide.

A study entitled “Potent anti-angiogenic motifs within the Alzheimer’s β-amyloid peptide” was published in the January 2008 issue of the journal Amyloid. Building on previous work showing that the Alzheimer’s Aβ peptide is able to prevent blood vessel growth and inhibit tumor growth, Roskamp Institute scientists investigated particular sequences within the Alzheimer’s Aβ peptide in order to identify whether short derivatives of Aβ are able to have the same effect. Inhibition of blood vessel growth is an attractive approach for preventing tumorigenesis since tumors need an adequate blood supply to grow beyond a certain size. Using different fragments of the Aβ peptide, we have identified, for the first time, a critical 8 amino acid sequence within the Aβ peptide, HHQKLVFF, which is able to block blood vessel growth. This short peptide has potential therapeutic relevance for the prevention of tumor growth. The Roskamp Institute specializes in Alzheimer’s Disease research and under the leadership of Dr Michael Mullan has focussed on the role of inflammation in Alzheimer’s Disease and on new treatments for Alzheimer’s Disease and other disorders. This work was a spin off of Mullan and colleagues’ Alzheimer research which has previously shown that the Alzheimer’s Disease peptide can adversely impact blood vessels in Alzheimer’s Disease and may contribute to the decline seen, for instance, after stroke in Alzheimer’s Disease patients.

For more details read the journal article at:
Patel NS, Quadros A, Brem S, Wotoczek-Obadia M, Mathura VS, Laporte V, Mullan M, Paris D. Amyloid. 2008 Mar;15(1):5-19.

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CD40L induces Abeta production via signaling by the granulocyte macrophage colony stimulating factor (GM-CSF): A note by Mullan

Alzheimer’s disease is the most common type of dementia in the elderly. Alzheimer’s Disease is mainly characterized by the accumulation of a small molecule (known as amyloid beta (Abeta) in the brain. Many researchers have shown that the molecule CD40L is elevated in Alzheimer’s Disease patients. Roskamp Institute research group headed by Dr. Michael Mullan also have shown that CD40L stimulation increases Abeta levels in cellular models of the disease. Furthermore, we have shown that CD40L stimulation of cells that are important for the defense of the nervous system induces increases in pro-inflammatory molecules known as cytokines. The granulocyte macrophage colony stimulating factor (GM-CSF) is one of these cytokines involved in inflammation responses in the brain. Numerous studies have correlated Alzheimer’s Disease with increases in pro-inflammatory cytokines. In the cytokine paper, we have shown that CD40L stimulation increases the levels of both GM-CSF and Abeta in Alzheimer’s Disease cell models. We have shown that treatment of these cells with GM-CSF causes a time dependent significant increase in Abeta levels. We demonstrate that blocking GM-CSF reduces CD40L-induced Abeta production in a dose dependent manner. In addition, we show that inhibiting GM-CSF signaling by silencing the GM-CSF receptor gene significantly reduces Abeta levels to below basal levels in non-CD40L-stimulated by blocking the trafficking of Abeta’s mother protein, the amyloid precursor protein. Our results that are now published in the Journal cytokine (Volmar et al., 2008) suggest that GM-CSF operates downstream of CD40/CD40L interaction and that GM-CSF modulates Abeta production. The Roskamp Institute specializes in Alzheimer’s Disease research and under the leadership of Dr Michael Mullan has focussed on the role of inflammation in Alzheimer’s Disease and on new treatments for Alzheimer’s Disease and other disorders. Mullan and colleagues have been examining ways to treat Alzheimer’s Disease by inhibiting the CD40 pathway.

The granulocyte macrophage colony stimulating factor (GM-CSF) regulates amyloid beta production (2008). Volmar CH, Ait-Ghezala G, Frieling J; Paris D, Mullan MJ Cytokine 42(3):336-44.

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Alzheimer Researcher Mike Mullan's note on:Potent antiangiogenic motif in amyloid beta

Roskamp Institute study entitled “Potent anti-angiogenic motifs within the Alzheimer’s β-amyloid peptide” was published in the January 2008 issue of the scientific journal Amyloid. Work by Dr. Michael Mullan and Dr. Daniel Paris showed that a protein central to Alzheimer’s disease pathology is also able to prevent blood vessel growth and stop tumors. In our current study, we investigated whether shorter versions of this same protein could have the same effect. By stopping the blood supply to a tumor, we can effectively starve it and stop cancer. In this study, we have identified a small protein that is able to halt blood vessel growth. Therefore, this short protein has great potential as a novel treatment for cancer. The Roskamp Institute specializes in Alzheimer’s Disease research and under the leadership of Dr Michael Mullan has focussed on the role of inflammation in Alzheimer’s Disease and on new treatments for Alzheimer’s Disease and other disorders. The work on the potential role of Aβ on tumor vessel growth arose out of studies by Drs. Paris, Mullan and colleagues suggesting that Aβ might negatively impact blood vessel growth in Alzheimer’s Disease. In particular Drs Paris and Mullan have shown that the Alzheimer’s Aβ increases the tendency of blood vessels to constrict and others have confirmed that this tendency may make the effects of stroke worse in Alzheimer’s Disease patients.

Potent anti-angiogenic motifs within the Alzheimer beta-amyloid peptide (2008). Patel N, Quadros A, Brem S, Wotoczek-Obadia M, Mathura V, Laporte V, Mullan M, Paris D Amyloid 15(1):5-19.

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Dr. Mullan's comment on The granulocyte macrophage-colony stimulating factor (GM-CSF) regulates amyloid production

Alzheimer disease is the most common cause of dementia, afflicting 24 million people worldwide. Over time, Alzheimer's disease gradually destroys a person's memory and ability to learn and carry out daily activities. In addition; individuals may also experience changes in personality and behavior. Alzheimer disease is accompanied by the presence of amyloid plaques and neurofibrillary tangles in the brain of Alzheimer's patients with increases in pro-inflammatory cytokines. Beta-amyloid (Alzheimer’s Aβ) is a key protein shown to play a central role in Alzheimer's disease etiology. Unfortunately, there is currently no known cure, finding a way to stop Alzheimer’s Aβ production and/or increase it degradation will lead to a potentially drug target that can be used to stop the disease. The granulocyte macrophage colony stimulating factor (GM-CSF) is a signaling protein used extensively in cellular communication. GM-CSF has been suggested to induce programmed cell death in the brain tissue of patients with Alzheimer’s Disease. Scientist at the Roskamp institute showed that blocking this protein reduce the production of the main pathological protein that causes Alzheimer's disease (Alzheimer’s Aβ ) below basal level. In addition the Roskamp Institute scientists examined the mechanism underlying Alzheimer’s Aβ reduction after silencing of the receptor protein of G-CSF. Their result show that these effect is due to the fact that blocking the GM-CSF receptor reduce APP (Beta-amyloid protein precursor) trafficking from the cell membrane to the inside of the cell were the preotein in cleaved to generate the Alzheimer’s Aβ fragment. The discovery is detailed in an article appears in the journal Cytokine. The Roskamp Institute specializes in Alzheimer’s Disease research and under the leadership of Dr Michael Mullan has focussed on the role of inflammation in Alzheimer’s Disease and on new treatments for Alzheimer’s Disease and other disorders. Mullan and colleagues have previously published papers showing that inflammatory molecules like CD40 adversely contribute to Alzheimer’s Disease that that blocking CD40 signaling could help prevent the pathology that occurs in Alzheimer’s Disease.

The granulocyte macrophage colony stimulating factor (GM-CSF) regulates amyloid beta production (2008). Volmar CH, Ait-Ghezala G, Frieling J; Paris D, Mullan MJ Cytokine 42(3):336-44.

Microglial activation resulting from CD40-CD40L interaction after beta-amyloid stimulation (1999). Tan J, Town T, Paris D, Mori T, Suo Z, Crawford F, Mattson MP, Flavell RA, Mullan M. Science, 286(5448):2352-5.

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Alzheimer Research Dr. Mullan's comment on Genetic manipulation of CD40L reduces Tau phosphorylation

Mainly two cerebral lesions characterized Alzheimer’s disease (AD): an extracellular deposition of the beta-amyloid peptide (Abeta) in senile plaques and an intracellular accumulation of neurofibrillary tangles (principally composed of protein tau). Besides these lesions, a continuous inflammatory state exists in the brain of AD patients.
In AD brains, the tau protein becomes hyper-phosphorylated and acquires a new three-dimensional conformation that results into its aggregation in neuronal cells to form neurofibrillary tangles (NFT). It is generally accepted that the accumulation of Abeta in senile plaques promotes the formation of NFT in AD.
The impact of cerebral inflammation on the aggregation of Abeta has been widely studied. At the Roskamp Institute, it has been previously shown that the binding of CD40 ligand (CD40L) to its receptor CD40, two protein mediating inflammation, is deleterious for AD. Indeed, in the transgenic mouse model for AD Tg2576, disruption of CD40-CD40L binding — by genetic deletion of either CD40 or CD40L, or by a pharmacological treatment — mitigates the amyloid deposition and the associated neuro-inflammation.
In a recent study to be published in Brain Research, the Roskamp Institute reports that the same genetic manipulation (CD40 or CD40L deficiency) in the Tg2576 mouse model for AD reduces the hyper-phosphorylation of the tau protein as well. Interestingly, these data suggest that this decrease is independent than that of Abeta deposition implying that CD40-CD40L pathway has a direct effect on the phosphorylation of tau. Because it would act on the two main pathological features of AD, the therapeutic interest of targeting this pathway is greatly increased by this discovery.

The Roskamp Institute specializes in Alzheimer’s Disease research and under the leadership of Dr Michael Mullan has focussed on the role of inflammation in Alzheimer’s Disease and on new treatments for Alzheimer’s Disease and other disorders.
Microglial activation resulting from CD40-CD40L interaction after beta-amyloid stimulation (1999). Tan J, Town T, Paris D, Mori T, Suo Z, Crawford F, Mattson MP, Flavell RA, Mullan M. Science, 286(5448):2352-5.

CD40 deficiency mitigates Alzheimer's disease pathology in transgenic mouse models (2006). Laporte V, Ait-Ghezala G, Volmar CH, Mullan M. J. Neuroinflammation. 2006 Feb 24;3(1):3

CD40 ligation mediates plaque-associated tau phosphorylation in beta-amyloid overproducing mice (2008). Laporte V, Ait-Ghezala G, Volmar CH, Ganey C, Ganey N, Wood M, Mullan M Brain Res. 1231:132-42.

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Dr. Mullan's Comment on Alzheimer’s and Blood Pressure

The relationship between blood pressure and Alzheimer’s disease is complex. However, we do know that blood pressure raised in mid-life (hypertension) is a risk for the development of Alzheimer’s disease later on. Uncontrolled hypertension is a risk for dementia in general. In fact, stroke related dementias are primarily caused by either clotting or small bleeds in the brain. Hypertension can lead to bleeding, primarily in the brain, but can also damage the heart triggering the release of small clots that lodge in the brain, thus depriving the nerve cells (neurons) of oxygen supply.

It remains unclear to scientists why hypertension is a risk for Alzheimer’s disease, but we do know that in spontaneously hypertensive rats, there is a tendency to accumulate some of the pathology of Alzheimer’s disease.

In 1996, researchers at the Roskamp Institute discovered that the causative protein in Alzheimer’s (the amyloid protein) has a drastic effect on blood vessels. The effect is to increase the propensity of blood vessels to constrict. Subsequently, others show that after a small stroke (when blood vessels close down temporarily) the presence of amyloid tends to keep the blood vessels closed. It is assumed that the consequence of reduced blood flow to the brain, secondary to closed blood vessels, causes deprivation of oxygen and glucose to the neurons, thus causing more damage in a brain with high amyloid levels than one with not.

Translated into clinical terms, this means that the effect of a small stroke on somebody who is in the early stages of Alzheimer’s can be more devastating than somebody who is not. In fact, a study of nuns who were asked to complete mental state questionnaires in life and who subsequently died has revealed an important interaction between small strokes and the clinical signs of Alzheimer’s. Even though some nuns had amyloid deposits in their brain, they did not exhibit the symptoms of amyloid in life. Those nuns that had amyloid deposits but did exhibit the clinical symptoms of Alzheimer’s in life also had multiple small strokes.

Thus, damage to the blood vessels in the presence of amyloid is more devastating than if amyloid is absent. Hypertension tends to damage blood vessels throughout the body, but it is only in the brain that amyloid accumulates and can contribute to poor recovery after vascular injury.

What does this mean for patients treated at the Roskamp Institute? Patients are advised to take particular care to have their blood pressure and cardiovascular status monitored. High lipid or triglyceride levels can contribute to cerebrovascular (brain/blood vessel) damage and uncontrolled or poorly monitored high hypertension can also be highly detrimental. In addition, we know that other cardiac problems, such as arrhythmias can contribute to cerebrovascular damage, as mentioned, by throwing off small clots.

As we await effective treatments to combat Alzheimer’s directly, we need to ensure that we control other disorders which can contribute significantly to rapid declines in mental status. Interestingly, some antihypertensives seem to be able to control the risk for Alzheimer’s disease as well as controlling blood pressure.

Researchers at the Roskamp Institute have clearly shown that this does not apply to all antihypertensives and they are investigating why some are able to regulate both blood pressure and can reduce the incidence of Alzheimer’s disease while others cannot. This is an important area of research and clearly one that holds out hope for Alzheimer’s sufferers as the search for new treatments continues.

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