Alzheimer's disease is a progressive neurodegenerative disease that is histopathologically characterized by the presence of plaques consisting mainly of Abeta amyloid and tangles, mainly of hyper phosphorylated tau. To date, no treatment can reverse the disease and all current therapeutics aimed at dealing with the disease's symptoms. Here we describe the efforts to attack the plaques and, in more detail, the process of neurofibrillary degeneration associated with the presence of the protein tau associated with hyper phosphorylated microtubules. We have identified the various targets and current knowledge for therapeutics.
Alzheimer's disease treatment enters a new and exciting phase with several new drugs that begin clinical studies. Many of these new therapies are based on our current best understanding of Alzheimer's disease pathogenesis and are designed to either slow or stop the disease's progression. The current efforts are based on several different theories, which are reviewed briefly. Therapies aimed at some aspects of beta - amyloid formation, neurofibrillary tangle formation and inflammatory response as well as the problems associated with each area are considered. Whether any of these approaches will be successful is still unclear, but the high level of activity in each of these three areas gives some hope that Alzheimer's disease will be treated effectively.
This session covers Abeta, truncated and pGlu-Abeta, immunotherapy, targets based on neurotransmitters, anti - inflammatory targets, nanotechnology, antioxidants, neurotropic factors, protein aggregation, brain stimulation, malfolding and chaperones, gene therapy, drug delivery systems.
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