Amyloid cascade hypothesis: Pathogenesis and therapeutic strategies in Alzheimer's disease |
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| Institution: | 1. Structural Bioinformatics Unit, Department of Biochemistry, Shivaji University, Kolhapur 416004, Maharashtra (M.S.), India;2. Department of Biotechnology, Shivaji University, Kolhapur 416004, Maharashtra (M.S.), India;3. Department of Microbiology, Shivaji University, Kolhapur 416004, Maharashtra (M.S.), India;1. Department of Neurology, University of Szeged, Semmelweis u. 6, Szeged H-6725, Hungary;2. MTA – SZTE Neuroscience Research Group, Semmelweis u. 6, Szeged H-6725, Hungary;1. Mitchell Center for Neurodegenerative Diseases, University of Texas Medical Branch, Galveston, TX 77555, USA;2. Department of Neurology, University of Texas Medical Branch, Galveston, TX 77555, USA;3. Department of Neuroscience and Cell Biology, University of Texas Medical Branch, Galveston, TX 77555, USA;4. Sealy Center for Vaccine Development, University of Texas Medical Branch, Galveston, TX 77555, USA |
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| Abstract: | Alzheimer's disease is an irreversible, progressive neurodegenerative disorder. Various therapeutic approaches are being used to improve the cholinergic neurotransmission, but their role in AD pathogenesis is still unknown. Although, an increase in tau protein concentration in CSF has been described in AD, but several issues remains unclear. Extensive and accurate analysis of CSF could be helpful to define presence of tau proteins in physiological conditions, or released during the progression of neurodegenerative disease. The amyloid cascade hypothesis postulates that the neurodegeneration in AD caused by abnormal accumulation of amyloid beta (Aβ) plaques in various areas of the brain. The amyloid hypothesis has continued to gain support over the last two decades, particularly from genetic studies. Therefore, current research progress in several areas of therapies shall provide an effective treatment to cure this devastating disease. This review critically evaluates general biochemical and physiological functions of Aβ directed therapeutics and their relevance. |
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