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NGF Signaling and Trafficking
Alzheimer's disease (AD) is an age-related, dementing disorder of unknown cause,
is the most common cause of dementia among the elderly, account for 60 to 80% of the cases,
with nearly 20 million cases predicted by 2050 in the US alone. Interestingly, Research has shown that by the age of 40,
nearly all Down Syndrome patients will develop symptoms of Alzheimers Disease.
We have been fortunate, through a wealth of collaborations, to study the basic mechanisms of Alzheimer and Down syndrome, two common diseases that provoke profound distress and chaos in the life of patients and their relatives. Interestingly, It is therefore clear that the understanding of the mechanisms governing the biology of the brain of subjects with a triplicated chromosome 21 will clarify many of the molecular events that arise during the development of Alzheimer disease. A key event in the
progress of Alzheimer's disease is the degeneration of cholinergic neurons in the basal forebrain and the subsequent acetylcholine deficit in the hippocampus, leading to memory loss. Our recent findings, using a mouse model that mimics the triplication of the chromosome 21 in humans, emphasize the complexity of those diseases and highlight the role of intracellular basic mechanisms. Following our findings on the
importance of axonal transport and nerve growth factor availability at the early stages of Down's syndrome, our goal has been to study in detail the role of individual genes within the triplicated chromosome and understand their involvement in the course of the disease
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