The American Journal of Pathology recently published research that offers important clues to doctors hoping to better understand why some people suffer from dementia and diseases like Alzheimer’s and others don’t.
Researchers discovered important differences in proteins between patients with dementia and those who were cognitively intact. The investigative team evaluated brain autopsy samples from different areas of the subjects’ brains. Four of the subjects were cognitively normal and elderly, two had spinocerebellar ataxia type II (a condition characterized by problems with balance, coordination, speech, and swallowing), 24 subjects were diagnosed with Alzheimer’s disease and clinical dementia, 15 subjects had no history of dementia but displayed signs of AD-related pathology.
“Our results suggest that effective therapies will need to target synaptic Aβ oligomers, and that anti-amyloid therapies will be much less effective once synaptic p-tau pathology has developed, thus providing a potential explanation for the failure of amyloid-based trials.” Karen H. Gylys, PhD, UCLA School of Nursing and the Mary S. Easton Center for Alzheimer’s Research at UCLA.
Tau-focused drug therapies
People with neurodegenerative diseases, also known as tauopathies (the most prevalent of which is Alzheimer’s disease) have misfolded tau as a key pathological agent. Tau-focused drug therapies set out to correct this malfunction in the development and transformation of brain cells.
Phase III clinical trials of amyloid-β-targeted therapeutics indicate some sort of mistake in the theory that correcting the misfolded tau could stop or even reverse symptoms of dementia. New studies underway seek new ways to compensate for the loss of normal tau function.
The theory often referred to as amyloid hypothesis in the medical community suggests that an imbalance in clearance and production of amyloid beta (Abeta) triggers events that lead to dementia and neurodegeneration.
Anti-Amyloid drugs that modify the body’s ability to produce and clear Abeta appear to work better in the early stages of dementia according to this new research from UCLA.
This approach was recently validated by the pharmaceutical company Biogen, in their Phase I human trial of a new Alzheimer’s drug.
“It is the first trial showing that lowering Abeta levels in the brain can slow down cognitive decline in patients. It also nicely dovetails with several active CAF projects. Most importantly, it further validates our understanding of the disease, from genetic studies, showing that amyloid plaques initiate the disease by causing the formation of neurofibrillary tangles and inflammation. The Biogen study offers the first proof that if you can stop the accumulation of Abeta in the brain, you can slow down or even stop the disease in its tracks.” Rudy Tanzi, Ph.D., chair of the Cure Alzheimer’s Fund (CAF) Research Consortium
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