Cholinotrophic molecular pathobiology during the onset of Alzheimer’s disease: Looking back to see the future
Data: Osteguna, urriaren 25ean
Laburpena
Alzheimer’s disease (AD) is characterized by a progressive phenotypic down regulation of markers within cholinergic basal forebrain (CBF) neurons, frank CBF cell loss and reduced cortical choline acetytransferase activity associated with cognitive decline. Delaying CBF neurodegeneration or minimizing its consequences is the mechanism of action for most currently available drug treatments for cognitive dysfunction in AD.
Growing evidence suggests that imbalances in the expression of nerve growth factor (NGF), proNGF, the high (TrkA) and low (p75NTR) affinity NGF receptors, tau aggregation and epigenetics are crucial factors underlying CBF dysfunction in AD. Here we will discuss the molecular and cellular pathobiology of these factors in relation to cholinergic forebrain survival and plasticity using tissue obtained from the Religious Orders Study, a clinical pathological longitudinal investigation of aging and AD.
Hizlaria
Elliott J. Mufson
Dr. Mufson (H-factor: 85) is a Professor of Neurobiology and Greening Chair in Neuroscience at the Barrow Neurological Institute, Phoenix, AZ is an expert in connectional and chemical neuroanatomy of normal and diseased brain. He trained at the Harvard Medical School in the Department of Neurology where he worked with Dr. M-M Mesulam to produce a series of classic papers on the connectivity of the non-human primate cholinergic system. He was Associate Director of the Sun Heath Research Institute, Sun City, AZ where he development of one of the most prestigious human brain banks in the USA.
He was recruited to Rush University Medical Center, Chicago, IL where he was instrumental in the development of NIA Rush Religious Order Study, a clinical pathological longitudinal investigation of aging and dementia. He pioneered the application of single cell expression profiling to human postmortem tissue. He is active in the fields of Down syndrome and CTE in the human brain. His translational research lead to clinical trials using neurotrophin therapy to treat AD and Parkinson’s disease.
He has published over 300 peer-reviewed articles. The Institute for Scientific Information recognized him as one of the 100 most highly cited researchers in neuroscience. NIA and DoD currently fund his research.