Therapeutic Targets

Alzheimer's disease is a progressive neurodegenerative disease that is characterized histopathologically by the presence of plaques, mainly composed of Abeta amyloid and the tangles, mainly composed of hyperphosphorylated tau. To date, there is no treatment that can reverse the disease, and all the current therapeutics is directed to cope with the symptoms of the disease. Here we describe the efforts dedicated to attack the plaques and, in more detail, the process of neurofibrillary degeneration, linked to the presence of the hyperphosphorylated microtubule associated protein tau. We have identified the different putative targets for therapeutics and the current knowledge on them.
 

Treatment for Alzheimer's disease is entering a new and exciting phase, with several new drugs beginning clinical trials. Many of these new therapies are based on our best current understanding of the pathogenesis of Alzheimer's disease, and are designed to try to either slow or halt the progression of the disease. There are several different theories underlying the current efforts, and these are briefly reviewed. Therapies directed against some aspect of beta-amyloid formation, against neurofibrillary tangle formation and against the inflammatory response are all considered, as are the problems associated with each area. It is as yet unclear which, if any, of these approaches will be successful, but the high level of activity in each of these three fields provides some hope that an effective treatment for Alzheimer's disease is on the horizon.

Research and development of new therapies for Alzheimer's disease are largely based on the observation that accumulation of peptide appears pivotal to the development of the disease. For maximum benefit, such therapies would have to be administered early on in the development of the disease. This relies upon improvement of diagnostic techniques. At present diagnosis is through the use of cognitive testing and observational scanning of the brain through use of the MRI techniques.

This session includes Abeta, truncated and pGlu-Abeta, Immunotherapy, Neurotransmitter-based targets, Anti-inflammatory targets, Nanotechnology, Anti-oxidants, Neurotrophic factors, Protein aggregation, Deep brain stimulation, Misfolding and chaperones, Gene therapy, Drug-delivery systems.
  • Abeta, truncated and pGlu-Abeta
  • Immunotherapy
  • Neurotransmitter-based targets
  • Anti-oxidants
  • Neurotrophic factors
  • Protein aggregation
  • Deep brain stimulation
  • Misfolding and chaperones
  • Gene therapy
  • Nanotechnology
  • Drug-delivery systems
  • Anti-inflammatory targets

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