2016IOSR Journal of Pharmacy and Biological SciencesOpen access

The Role of M1/M2 Transition of the Brain Macrophages in Alzheimer’s Disease

Neha Milind Chitre, Priya J. Ghumatkar, Sadhana S. Sathaye

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Abstract

Alzheimer's disease (AD) is a neurodegenerative disorder that is characterized by the presence of neurofibrillary tangles (NFT) and senile plaques caused due to amyloid beta (Aβ) aggregation in the brain.Macrophage like resident immune cells in the brain called microglia play a pivotal role in the CNS immunity.They are constantly engaged in removing damaged cells which is a very important part of maintaining homeostasis.Microglial cells contribute to the clearance of Aβ by the process of phagocytosis, which may lead to delaying the progression of AD.Microglial cells also exhibit their neuroprotective role by secreting various growth factors.However, hyper activation of microglia leads to a sustained overproduction of microglial proinflammatory mediators which are neurotoxic and which raise great concern that systemic inflammation can exacerbate or possibly trigger neurological diseases.The aim of the present study is to unravel the dual role of microglia by studying the macrophage M1/ M2 Polarization and to further exploit this link in implicating newer therapeutic interventions.

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Alzheimer's disease (AD) is a neurodegenerative disorder that is characterized by the presence of neurofibrillary tangles (NFT) and senile plaques caused due to amyloid beta (Aβ) aggregation in the brain.Macrophage like resident immune cells in the brain called microglia play a pivotal role in the CNS immunity.They are constantly engaged in removing damaged cells which is a very important part of maintaining homeostasis.Microglial cells contribute to the clearance of Aβ by the process of phagocytosis, which may lead to delaying the progression of AD.Microglial cells also exhibit their neuroprotective role by secreting various growth factors.However, hyper activation of microglia leads to a sustained overproduction of microglial proinflammatory mediators which are neurotoxic and which raise great concern that systemic inflammation can exacerbate or possibly trigger neurological diseases.The aim of the present study is to unravel the dual role of microglia by studying the macrophage M1/ M2 Polarization and to further exploit this link in implicating newer therapeutic interventions.

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Available abstract

Alzheimer's disease (AD) is a neurodegenerative disorder that is characterized by the presence of neurofibrillary tangles (NFT) and senile plaques caused due to amyloid beta (Aβ) aggregation in the brain.Macrophage like resident immune cells in the brain called microglia play a pivotal role in the CNS immunity.They are constantly engaged in removing damaged cells which is a very important part of maintaining homeostasis.Microglial cells contribute to the clearance of Aβ by the process of phagocytosis, which may lead to delaying the progression of AD.Microglial cells also exhibit their neuroprotective role by secreting various growth factors.However, hyper activation of microglia leads to a sustained overproduction of microglial proinflammatory mediators which are neurotoxic and which raise great concern that systemic inflammation can exacerbate or possibly trigger neurological diseases.The aim of the present study is to unravel the dual role of microglia by studying the macrophage M1/ M2 Polarization and to further exploit this link in implicating newer therapeutic interventions.

Key concepts: Microglia, Neuroprotection, Inflammation, Proinflammatory cytokine, Neuroscience, Neuroinflammation, Macrophage, Immune system

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