Alzheimers disease (AD) is the most common age-associated neurodegenerative disease in the world. The major neuropathological features of AD are synaptic loss, neuronal loss, neurofibrillary tangles and the deposition of amyloid- β (Aβ) as plaques and in cerebral blood vessels. Numerous Aβ targeting therapeutic approaches have been shown to prevent amyloid deposition and resulting in cognitive improvement in transgenic mouse models of AD. Some of these approaches are currently in early clinical trials. It remains to be seen if these approaches will be proven effective in patients. Future anti-AD therapies will likely be multi-modal and individually tailored depending on the patients immune status, genetic background and their amyloid burden, as determined by imaging studies using Aβ specific labeling ligands. Preclinical data suggests that it will be much more feasible to prevent AD related pathology, then to clear existing pathology, making early diagnosis critically important.
Keywords: neurotoxicity, CNS neurons, RAGE-mediated transport, tau phosphorylation, Amyloid beta Deposition
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