Abstract
Alzheimers Disease (AD) physiopathology is not yet totally established. Nevertheless it is known that a metabolism dysfunction of the amyloid beta precursor protein (APP) and the abnormal tau protein phosphorylation lead to the formation of neuritic plaques and neurofibrillary tangles, respectively. These events finally drive to the clinical expression of dementia. Formally approved during the past decade, treatments for AD are lacking of an updating, being essentially symptomatic. Anticholinesterase agents have failed in providing a substantial improvement in the mental health condition of AD patients. On the other hand, antiamyloid strategies, have failed in their efficacy or security on their last development phases. In this context, tau represents a potential therapeutic target, by the action of drugs that diminish its aggregation, or acting by altering its phosphorylation or filaments formation. There is also anti-tau miscellaneous strategies such as normal microtubule-stabilizing agents. Thus, it might be possible that in a near future the neurodegenerative process could be stopped.
Keywords: Alzheimer's disease, disease tratement avenues, tau protein, anti-tau agents, tau pathology, clinical correlations, donepezil, NMDA receptor, ChEIs, 3xTg-AD, intracellular proteins, sequestration, NAP, ICC, GSK-3, CLK-2, HEB, polyubiquitinate tau
Current Alzheimer Research
Title: A Clinical Perspective: Anti Taus Treatment in Alzheimers Disease
Volume: 8 Issue: 6
Author(s): P. Fuentes and J. Catalan
Affiliation:
Keywords: Alzheimer's disease, disease tratement avenues, tau protein, anti-tau agents, tau pathology, clinical correlations, donepezil, NMDA receptor, ChEIs, 3xTg-AD, intracellular proteins, sequestration, NAP, ICC, GSK-3, CLK-2, HEB, polyubiquitinate tau
Abstract: Alzheimers Disease (AD) physiopathology is not yet totally established. Nevertheless it is known that a metabolism dysfunction of the amyloid beta precursor protein (APP) and the abnormal tau protein phosphorylation lead to the formation of neuritic plaques and neurofibrillary tangles, respectively. These events finally drive to the clinical expression of dementia. Formally approved during the past decade, treatments for AD are lacking of an updating, being essentially symptomatic. Anticholinesterase agents have failed in providing a substantial improvement in the mental health condition of AD patients. On the other hand, antiamyloid strategies, have failed in their efficacy or security on their last development phases. In this context, tau represents a potential therapeutic target, by the action of drugs that diminish its aggregation, or acting by altering its phosphorylation or filaments formation. There is also anti-tau miscellaneous strategies such as normal microtubule-stabilizing agents. Thus, it might be possible that in a near future the neurodegenerative process could be stopped.
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Cite this article as:
Fuentes P. and Catalan J., A Clinical Perspective: Anti Taus Treatment in Alzheimers Disease, Current Alzheimer Research 2011; 8 (6) . https://dx.doi.org/10.2174/156720511796717221
DOI https://dx.doi.org/10.2174/156720511796717221 |
Print ISSN 1567-2050 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-5828 |
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