Polyglutamine Disorders (Huntington's, etc.), Alzheimer Disease, Prion Diseases, Tauopathies, Parkinson Disease, Stroke and Trauma, Aging Process
Animal Models, Molecular and Cell biology, Neurobiology, Neuroimmunology, Brain imaging, Neuropathology, Chemistry/Pharmacology, Clinical trials, Oxidative Stress, Drug screening, Signal transduction, A-beta PP/A-beta, Tau/Cytoskeleton
Researcher Bio To be attached
Top Papers To be attached
What is your leading hypothesis? The Amyloid Cascade Hypothesis remains the driving hypothesis for my research team's efforts
What piece of missing evidence would help prove it? I think by now that one's belief in the Amyloid Hypothesis is an article of faith. You either accept it or you don't.
The issue will only be settled by the outcomes of well-designed clinical trials with therapeutics targeted at aspects of the amyloid hypothesis.
What is your fallback position? Neurofibrillary tangle pathology is the other major hallmark of AD. The recent discovery of familial Tauopathies has definitively proven the role that dementia can be directly caused by mis-metabolism of tau.
Neuroinflammation and oxidative stress also appear to play a significant role in pathogenesis, although these processes are not unique to AD.