Alzheimer's disease is the most common cause of dementia, accounting for up to 70 percent of all cases. But it's not the only one -- Lewy body dementia, frontotemporal degeneration (FTD), vascular dementia, and others affect thousands of Americans.
Research has shown that many forms of dementia -- and neurodegenerative diseases such as ALS and Huntington's -- share some of the same underlying causes as Alzheimer's disease. So treatments for one type of brain disease could potentially be effective at treating others.
Vascular dementia, the second most common form in the elderly, is caused by strokes and "mini-strokes" that damage the brain's large and small blood vessels. Most Alzheimer's patients also have vascular disease, and impaired blood flow in key brain areas is common in Alzheimer's and other dementias.
Lewy body dementia is the third most common type in older people. The alpha-synuclein protein, a Lewy body, prevents the normal functioning of the brain. Lewy bodies are also present in Parkinson's disease patients.
FTD, which encompasses several distinct diseases including progressive supranuclear palsy, is often marked by tau tangles, which also play a major role in destroying neurons (brain cells) in Alzheimer's disease. TDP-43, a neurotoxic protein, is present in the brains of some patients with FTD, Alzheimer's, and ALS.
Neuroinflammation can be a contributing factor in many brain diseases. And neuroprotection strategies aim to protect neurons from damage. Drugs targeting either of these factors could potentially treat a wide range of brain diseases and disorders.
The Alzheimer's Drug Discovery Foundation (ADDF), where I am executive director, is funding drugs targeting these causes of dementia. Dr. Atticus Hainsworth, at St. George's, University of London, is repurposing the FDA-approved drug tadalafil to slow the progression of vascular cognitive impairment, a condition that precedes dementia. Dr. Frank Longo of Stanford University and the biotech PharmatrophiX is developing a neuroprotective drug that send signals to neurons that help them survive. Dr. D. Martin Watterson and his colleagues at Northwestern University are working on a new class of drugs that targets brain inflammation in Alzheimer's, traumatic brain injury, and multiple sclerosis. And, through our longstanding partnership with The Association for Frontotemporal Degeneration (AFTD), we are funding numerous drugs targeting tau and TDP-43.
But new drugs will only help patients if they have the right diagnosis. That's why we are also committed to investing in biomarkers and neuroimaging tests that can conclusively identify the hallmarks of these diseases and track their progression.
The ADDF has made a significant investment in the discovery of biomarkers that can identify and follow the progression of Alzheimer's, FTD and other dementias, and differentiate these diseases at an early stage. Dr. Mari DeMarco at the University of British Columbia is developing a way to detect TDP-43 and tau in cerebrospinal fluid. Dr. Neil Vasdev at Massachusetts General Hospital is conducting clinical trials of a new PET scan for tau proteins. And Dr. Keith St. Lawrence at Lawson Health Research Institute is using arterial spin labeling (an MRI technique) to assess the progression of FTD and possibly differentiate between its varying types.
It is my hope that the efforts of these and other pioneering researchers will soon succeed at providing effective therapies and diagnostic tools so we can end the devastating effects of Alzheimer's and related dementias.