Heart Disease May Hold Clues to Alzheimer’s Disease

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alzheimers-association-logo1On December 2014, scientific experts in the fields of both cardiovascular diseases and Alzheimer’s disease (AD) met in Chicago to discuss the link between vascular risk factors and dementia in AD. The event was organized by the Alzheimer’s Association, with scientific input from the National Institutes of Health’s National Institute of Neurological Disorders and Stroke (NINDS) and National Heart, Lung and Blood Institute (NHLBI). A review article, titled, “Vascular contributions to cognitive impairment and dementia including Alzheimer’s disease“, summarizes the meeting views and further research directions, and is available in advance online publication by Alzheimer’s & Dementia: The Journal of the Alzheimer’s Association.

“We are encouraged by the potential for new treatment strategies for dementia to arise from studying the crossover of vascular factors with the progression of Alzheimer’s,” says Heather M. Snyder, Ph.D., director of medical and scientific operations for the Alzheimer’s Association, and first author of the article.

Half of the people who die from AD have vascular lesions resulting from stroke. Brain imaging studies show a close association between vascular injury and cognitive decline in patients. One hypothesis is that vascular impairment in the brain accelerates beta–amyloid deposition, a hallmark of AD, enhancing the pathology and dementia in individuals with AD.  In addition, any changes in blood flow can affect brain cells.

“Blood vessels that deliver nutrients to the brain and carry away waste are vital for normal cognitive function,” says co-author Roderick Corriveau. Other comorbid conditions in AD patients may lead to vascular pathology and related dementia including hypertension, diabetes, hypercholesterolemia, obesity, low physical activity, depression, and smoking. Although, many of these diseases can be prevented by drugs and changes in lifestyle, further research is required to understand whether these drugs also reduce cognitive impairment in AD.

The participants in the meeting agreed that there is a need for new animal models that reproduce vascular injury together with AD pathology. In addition, new biological markers are necessary to understand the association between disease progression, impairment of brain function and key vascular processes. Together with new experimental models and tools, researchers should focus in understanding the mechanisms underlying brain blood flow decrease in AD and other dementias. Moreover, the effects of interventions to control vascular risk factors on cognition need to be addressed.

“Having the methods to detect early signs of vascular-related brain injury or disease with the greatest impact on Alzheimer’s and dementia would greatly enhance our efforts to develop effective therapies,” says David Knopman, also a co-author of the article.

The authors have also called attention to the need for national and international funding to further conduct research in this area. To wit, the Alzheimer’s Association recently launched a targeted grant program encouraging additional commitment to research the vascular contribution to dementia.