effect of N acetyl cysteine in intracerebroventricular colchicine induced cognitive deficits, beta amyloid pathology, and Glial cells

research article

Research output: Contribution to specialist publicationArticle

Abstract

among the many factors responsible for the cognitive decline in Alzheimer's disease, beta amyloid protein and plaque formation is crucial. the antioxidant NAC has reversed the cognitive deficits and inhibits the microglial activation. it can be postulated that NAC might have reversed the effect of intraneuronal beta amyloid protein by acting on some downstream compensatory mechanism which needs to be explored.
Original languageEnglish
Number of pages15
Specialist publicationJournal of Neuroscience
Publication statusPublished - 2019

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Amyloid beta-Peptides
Colchicine
Amyloid
Neuroglia
Cysteine
Pathology
Amyloid Plaques
Research
Alzheimer Disease
Antioxidants
Cognitive Dysfunction

Cite this

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title = "effect of N acetyl cysteine in intracerebroventricular colchicine induced cognitive deficits, beta amyloid pathology, and Glial cells: research article",
abstract = "among the many factors responsible for the cognitive decline in Alzheimer's disease, beta amyloid protein and plaque formation is crucial. the antioxidant NAC has reversed the cognitive deficits and inhibits the microglial activation. it can be postulated that NAC might have reversed the effect of intraneuronal beta amyloid protein by acting on some downstream compensatory mechanism which needs to be explored.",
author = "Teresa Joy",
year = "2019",
language = "English",
journal = "Journal of Neuroscience",
issn = "0270-6474",
publisher = "Society for Neuroscience",

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T2 - research article

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AB - among the many factors responsible for the cognitive decline in Alzheimer's disease, beta amyloid protein and plaque formation is crucial. the antioxidant NAC has reversed the cognitive deficits and inhibits the microglial activation. it can be postulated that NAC might have reversed the effect of intraneuronal beta amyloid protein by acting on some downstream compensatory mechanism which needs to be explored.

M3 - Article

JO - Journal of Neuroscience

JF - Journal of Neuroscience

SN - 0270-6474

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