Research has shown that nearly two-thirds of dementia cases of patients over 60 in the Western Hemisphere are cases caused by Alzheimer’s disease.  This correlation with age continues as the frequency of Alzheimer’s nearly doubles by five year increments after the age of 65.To gain a better understanding of this prevalence, scientists are looking into the amyloid-b precursor protein (APP) gene which has shown to have a significant effect in those with Alzheimer’s disease.  Through their research, derived from 1,795 Icelandic citizens, scientists have discovered a mutation in the APP gene that safeguards individuals from cognitive deterioration and Alzheimer’s disease. Because mutations on this site (A673T allele) also prevents cognitive decline in patients without Alzheimer’s, this suggests that the two conditions may be controlled by or related through the same mechanisms. 

Patients enrolled in this study were registered through the Memory Clinic at Landspitali University Hospital and the cognitive condition was assessed through the Minimum Data Set (MDS) for nursing homes.  Genotypic data was then collects for the APP site A673T for all 1,763 patients.  This data reveals that this site on APP is vital to the production of amyloid plaque, making it able to protect patients from the cognitive decline seen in Alzheimer’s and non-Alzheimer’s patients.  These results make this mutation the first genetic variant discovered that can create a strong shield from Alzheimer’s disease.  It also confirms  the hypothesis that the pathogenesis of regular cognitive deterioration and Alzheimer’s disease may be partially related, suggesting that Alzheimer’s disease may be the driving force of the correlation between age and decline in cognitive function.

By Alec Waid, Intern Roskamp Institute
_  A groundbreaking new test for the early detection of Alzheimer's disease is being developed at a research facility just north of Sydney, Australia.  Currently, the only prevalent tests of such             nature are invasive and expensive.  However, the test being developed in Syndey is a cheap       blood test that checks for a change in levels of a specific protein marker over a year in order to      determine if a patient is in deed affected by the lethal disease.  The earlier Alzheimer's is   detected, the more likely it can be slowed and even stopped. To learn more about Biomarkers and clinical symptoms of Alzheimer's Disease please visit Dr. Michael Mullan Roskamp Institute home page

_ Researchers have shown that elevated pulse pressures in older humans with Alzheimer's disease    are at a higher risk to get Cerebrovascular disease. Recent studies have shown that patients with Alzheimer's disease that have a high pulse pressure may impair the clearance of beta-amyloid from the brain. Other studies show that high pulse pressures increases the chance of           Cerebrovascular disease which contributes to the cause of Alzheimer's disease. To learn more about cerebrovascular link to Alzheimer's disease please visit Roskamp Institute website.

_ A new study shows that reducing the iron levels in blood plasma may help protect the brain from changes. There is previous evidence that there are changes in the way the  human body  handles iron and other metals (zinc, cooper) before it shows Alzheimer's symptoms. In the             study, rats are fed a high cholesterol diet which causes them to build up plaques of a protein called beta-amyloid and develop changes in the tau proteins. The study deals with a new drug called deferiprone which lowered the iron concentration in the blood plasma of the rabbit and        the level of beta-amyloid and the tau proteins in the brain.  To learn more about work related to this at the Roskamp Institute please visit:


_  A new technology, recently approved by the FDA, allows researchers to detect amyloid plaques that often suggest Alzheimer's disease.  Created by Eli Lilly, Amyvid is a drug that, when used before a PET scan, will highlight amyloid plaque in the brain.  This method is much more preferable for diagnosis than the current method of performing an autopsy.

Alzheimer’s disease is a progressive neurodegenerative disorder that, until recently, has had very few treatment options, most of which do not generally target the underlying causes of the disease.  However, throughout the past decade, several case studies have revealed a possible treatment that is thought to slow the cause of this degenerative disorder: exercise.  In one circumstance, published in The Journal of Neuroscience (The Journal of Neuroscience, 27 April 2005, 25(17): 4217-4221; doi: 10.1523/​JNEUROSCI.0496-05.2005), after five months of exercise, amounts of extracellular amyloid-β plaque in the brain (specifically in the frontal cortex and the hippocampus) are decreased substantially in mice.  This change is believed to be brought about by neuronal metabolic alterations that affect the processing of the amyloid precursor protein which is believed to be responsible for the production of the amyloid- β plaque that, in Alzheimer’s patients, builds up in the brain, causing cognitive degradation. 

            At the University of Washington in Seattle, researchers have taken this theory from mice to human patients in an extensive study on the effects of exercise on Alzheimer’s disease and have contracted similar results.  According to Dr. Jeffrey Kaye, “…the challenge now, is to understand, at a scientific level, what elements really do enhance brain function, and what level, what dose of activity is needed.” According to the studies at the University of Washington, not just any exercise will do; 23 of the 33 volunteers, who were involved in an intense aerobic program, showed increase in cognitive abilities while the remaining 10, involved in non-aerobic stretching and balance exercises, continued to demonstrate the degrading symptoms of Alzheimer’s. 

            While the research and knowledge of the true effects of exercise on Alzheimer’s patients is still relatively young, there is a universal encouragement from the scientific community for those affected by Alzheimer’s to remain physically active for the better of their condition.  As research pertaining to this phenomenon continues to expand and develop and more is understood about the biological factors involved, there is a great potential for a treatment, possibly even a cure, of Alzheimer’s disease to be developed utilizing the methods of one of the most primitive of human activities: exercise.

Article by Roskamp Institute Inter Alec Waid.

To learn about Dr. Michael Mullan's research at the Roskamp Institute please visit: