TY - JOUR
T1 - The potential role of cytokines and growth factors in the pathogenesis of alzheimer’s disease
AU - Ogunmokun, Gilbert
AU - Dewanjee, Saikat
AU - Chakraborty, Pratik
AU - Valupadas, Chandrasekhar
AU - Chaudhary, Anupama
AU - Kolli, Viswakalyan
AU - Anand, Uttpal
AU - Vallamkondu, Jayalakshmi
AU - Goel, Parul
AU - Paluru, Hari Prasad Reddy
AU - Gill, Kiran Dip
AU - Reddy, P. Hemachandra
AU - De Feo, Vincenzo
AU - Kandimalla, Ramesh
N1 - Publisher Copyright:
© 2021 by the authors. Licensee MDPI, Basel, Switzerland.
PY - 2021/10/1
Y1 - 2021/10/1
N2 - Alzheimer’s disease (AD) is one of the most prominent neurodegenerative diseases, which impairs cognitive function in afflicted individuals. AD results in gradual decay of neuronal function as a consequence of diverse degenerating events. Several neuroimmune players (such as cytokines and growth factors that are key players in maintaining CNS homeostasis) turn aberrant during crosstalk between the innate and adaptive immunities. This aberrance underlies neuroinflammation and drives neuronal cells toward apoptotic decline. Neuroinflammation involves microglial activation and has been shown to exacerbate AD. This review attempted to elucidate the role of cytokines, growth factors, and associated mechanisms implicated in the course of AD, especially with neu-roinflammation. We also evaluated the propensities and specific mechanism(s) of cytokines and growth factors impacting neuron upon apoptotic decline and further shed light on the availability and accessibility of cytokines across the blood-brain barrier and choroid plexus in AD pathophysi-ology. The pathogenic and the protective roles of macrophage migration and inhibitory factors, neu-rotrophic factors, hematopoietic-related growth factors, TAU phosphorylation, advanced glycation end products, complement system, and glial cells in AD and neuropsychiatric pathology were also discussed. Taken together, the emerging roles of these factors in AD pathology emphasize the im-portance of building novel strategies for an effective therapeutic/neuropsychiatric management of AD in clinics.
AB - Alzheimer’s disease (AD) is one of the most prominent neurodegenerative diseases, which impairs cognitive function in afflicted individuals. AD results in gradual decay of neuronal function as a consequence of diverse degenerating events. Several neuroimmune players (such as cytokines and growth factors that are key players in maintaining CNS homeostasis) turn aberrant during crosstalk between the innate and adaptive immunities. This aberrance underlies neuroinflammation and drives neuronal cells toward apoptotic decline. Neuroinflammation involves microglial activation and has been shown to exacerbate AD. This review attempted to elucidate the role of cytokines, growth factors, and associated mechanisms implicated in the course of AD, especially with neu-roinflammation. We also evaluated the propensities and specific mechanism(s) of cytokines and growth factors impacting neuron upon apoptotic decline and further shed light on the availability and accessibility of cytokines across the blood-brain barrier and choroid plexus in AD pathophysi-ology. The pathogenic and the protective roles of macrophage migration and inhibitory factors, neu-rotrophic factors, hematopoietic-related growth factors, TAU phosphorylation, advanced glycation end products, complement system, and glial cells in AD and neuropsychiatric pathology were also discussed. Taken together, the emerging roles of these factors in AD pathology emphasize the im-portance of building novel strategies for an effective therapeutic/neuropsychiatric management of AD in clinics.
KW - Alzheimer’s disease
KW - Blood brain barrier
KW - Brain health
KW - Chemokines
KW - Cytokines
KW - Mild cognitive impairment
KW - Neuroinflammation
KW - Neurotrophic factors
KW - Pathophysiology
KW - Therapeutics
UR - http://www.scopus.com/inward/record.url?scp=85117124593&partnerID=8YFLogxK
U2 - 10.3390/cells10102790
DO - 10.3390/cells10102790
M3 - Review article
C2 - 34685770
AN - SCOPUS:85117124593
SN - 2073-4409
VL - 10
JO - Cells
JF - Cells
IS - 10
M1 - 2790
ER -