Mechanisms Involved in Microglial-Interceded Alzheimer's Disease and Nanocarrier-Based Treatment Approaches

Alzheimer's disease (AD) is a common neurodegenerative disorder accountable for dementia and cognitive dysfunction. The etiology of AD is complex and multifactorial in origin. The formation and deposition of amyloid-beta (Aβ), hyperphosphorylated tau protein, neuroinflammation, persistent oxida...

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Bibliographic Details
Published in:Journal of personalized medicine 2021-10, Vol.11 (11), p.1116
Main Authors: Md, Shadab, Alhakamy, Nabil A, Alfaleh, Mohamed A, Afzal, Obaid, Altamimi, Abdulmalik S A, Iqubal, Ashif, Shaik, Rasheed A
Format: Article
Language:English
Subjects:
Alzheimer's disease
Bioavailability
Cognitive ability
Cytokines
Dementia
Dementia disorders
Drug delivery
Drugs
Etiology
FDA approval
Immunogenicity
Inflammation
MAP kinase
Metabolism
Microglial cells
Neurodegenerative diseases
Neuromodulation
Neurotoxicity
Neurotransmitters
NF-κB protein
Oxidative stress
Pathogenesis
Pathology
Precision medicine
Proteins
Quality of life
Review
Synaptic plasticity
Tau protein
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Summary:Alzheimer's disease (AD) is a common neurodegenerative disorder accountable for dementia and cognitive dysfunction. The etiology of AD is complex and multifactorial in origin. The formation and deposition of amyloid-beta (Aβ), hyperphosphorylated tau protein, neuroinflammation, persistent oxidative stress, and alteration in signaling pathways have been extensively explored among the various etiological hallmarks. However, more recently, the immunogenic regulation of AD has been identified, and macroglial activation is considered a limiting factor in its etiological cascade. Macroglial activation causes neuroinflammation via modulation of the NLRP3/NF-kB/p38 MAPKs pathway and is also involved in tau pathology via modulation of the GSK-3β/p38 MAPK pathways. Additionally, microglial activation contributes to the discrete release of neurotransmitters and an altered neuronal synaptic plasticity. Therefore, activated microglial cells appear to be an emerging target for managing and treating AD. This review article discussed the pathology of microglial activation in AD and the role of various nanocarrier-based anti-Alzeihmenr's therapeutic approaches that can either reverse or inhibit this activation. Thus, as a targeted drug delivery system, nanocarrier approaches could emerge as a novel means to overcome existing AD therapy limitations.
ISSN:2075-4426
2075-4426
DOI:10.3390/jpm11111116