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Role of Retinoids in Treatment of Alzheimer's Disease


Affiliations
1 KCT's Ravindra Gambhirrao Sapkal College of Pharmacy, Anjaneri, Nashik-13, India
     

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Alzheimers disease very basically is characterized by the loss of the cognitive functions. β-amyloid is a major histopathological hallmark of Alzheimer's disease (AD). The disease is characterized by extracellular neuritic plaque composed of fibrillar-amyloid peptide and intracellular neurofibrillary tangles containing hyperphosphorylated tau. The peptides are generated by successive proteolysis of beta amyloid precursor protein, a large transmembrane glycoprotein that is initially cleaved by the site amyloid precursor protein cleaving enzyme -1 and subsequently by gamma secretase in the transmembrane domain. Retinoic acid is active metabolite of Vitamin A. Deprivation of Vitamin A results in amyloid-β accumulation, loss of hippocampal long term potentiation and memory deficit, all of which are hall mark of Alzheimers disease. Here we focused a role of retinoic acid on different pathophysiological features of Alzheimers disease. Retinoic acid may play an active role in treating neurodegenerative disorder. Retinoids appear to normalize many pathological states, and clinical side effects presently reported are mostly not serious except for retinoic acid syndrome.

Keywords

Alzheimers, Retinoic Acid, Vitamin A, Amyloid-β, Retinoid X Receptor(RXR).
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  • Role of Retinoids in Treatment of Alzheimer's Disease

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Authors

R. B. Saudagar
KCT's Ravindra Gambhirrao Sapkal College of Pharmacy, Anjaneri, Nashik-13, India
V. V. Buchake
KCT's Ravindra Gambhirrao Sapkal College of Pharmacy, Anjaneri, Nashik-13, India
R. S. Bachhav
KCT's Ravindra Gambhirrao Sapkal College of Pharmacy, Anjaneri, Nashik-13, India

Abstract


Alzheimers disease very basically is characterized by the loss of the cognitive functions. β-amyloid is a major histopathological hallmark of Alzheimer's disease (AD). The disease is characterized by extracellular neuritic plaque composed of fibrillar-amyloid peptide and intracellular neurofibrillary tangles containing hyperphosphorylated tau. The peptides are generated by successive proteolysis of beta amyloid precursor protein, a large transmembrane glycoprotein that is initially cleaved by the site amyloid precursor protein cleaving enzyme -1 and subsequently by gamma secretase in the transmembrane domain. Retinoic acid is active metabolite of Vitamin A. Deprivation of Vitamin A results in amyloid-β accumulation, loss of hippocampal long term potentiation and memory deficit, all of which are hall mark of Alzheimers disease. Here we focused a role of retinoic acid on different pathophysiological features of Alzheimers disease. Retinoic acid may play an active role in treating neurodegenerative disorder. Retinoids appear to normalize many pathological states, and clinical side effects presently reported are mostly not serious except for retinoic acid syndrome.

Keywords


Alzheimers, Retinoic Acid, Vitamin A, Amyloid-β, Retinoid X Receptor(RXR).

References