Alzheimer’s Disease:Intracellular Beta Amyloid Completes the Irreversible Pathway from Spirochetes to Biofilms to Beta Amyloid to Hyperphosphorylated Tau Protein

Hb, Allen; Rm, Allawh; Ca, Cusack; Sg, Joshi

doi:10.4172/2314-7326.1000276

Cited by 2 publications

(2 citation statements)

References 14 publications

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“…Neurotrophin receptor protein, regulates phosphorylation of TAU [71,72] In the case of AD, Aβ originating from APP trigger the rest of the pathologies. Aβ outside the neurons and neurofibrillary tangles inside the neurons make up for the development of AD [77,78]. Aβ further produces immune response activating complement systems.…”

Section: Immune System In Ad and Cytokinesmentioning

confidence: 99%

The Potential Role of Cytokines and Growth Factors in the Pathogenesis of Alzheimer’s Disease

Ogunmokun,

Dewanjee,

Chakraborty

et al. 2021

Cells

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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 neuroinflammation. 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 pathophysiology. The pathogenic and the protective roles of macrophage migration and inhibitory factors, neurotrophic 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 importance of building novel strategies for an effective therapeutic/neuropsychiatric management of AD in clinics.

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Section: Immune System In Ad and Cytokinesmentioning

confidence: 99%

The Potential Role of Cytokines and Growth Factors in the Pathogenesis of Alzheimer’s Disease

Ogunmokun,

Dewanjee,

Chakraborty

et al. 2021

Cells

View full text Add to dashboard Cite

show abstract

“…In the case of AD, β amyloids originating from APP trigger the rest of the pathologies. β amyloids outside the neurons and neurofibrillary tangles inside the neurons make up for the development of AD [6,7]. β amyloids, in turn, produce immune response activating complement systems.…”

Section: Immune Response In Ad: Role Of Cytokinesmentioning

confidence: 99%

The Potential Role of Cytokines and Growth Factors in the Pathogenesis of Alzheimer’s Disease

Ogunmokun¹,

Dewanjee²,

Chakraborty³

et al. 2021

Preprint

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Alzheimer’s disease (AD) is a neurodegenerative disorder characterized mainly by the gradual decay in neuronal function as a consequence of diverse degenerating events primarily including mitochondria dysfunction and cascades of neuro-immune reactions. Besides the acquired harmful reactive oxygen species (ROS), neurotoxins, and amyloid-beta (Aβ) and TAU pathologies in neurons, accumulating evidence with time underlined the roles of cytokines and growth factors in the AD pathogenesis. It may help us in evaluating the propensities and specific mechanism(s) of cytokines and factors impacting neuron upon apoptotic decline. Proinflammatory cytokines often induce inflammation in AD and AD-like pathogenesis in response to the apoptotic scenarios where some growth factors are involved in cytokinetic reactions to activate microglia and causing inflammation in AD. In this report, we comprehensively reviewed role of cytokines and chemokines in immune response to AD and neuropsychiatry. We provided insights into the neuroinflammation and the role of diverse factors including the pro-/anti-inflammatory cytokines, APP, TAU phosphorylation, glycation end products, complement system, and the role of glial cells. Also, we discussed the pathogenic and protective role of macrophage migration inhibitory factors, choroid plexus-, neurotrophic- and hematopoietic -related growth factors in AD. We further shed light on the availability and accessibility of the cytokines across the blood-brain barrier in AD pathophysiology. Taken together, the emerging role of these factors in AD pathology emphasized the importance of building novel strategies for an effective therapeutic/neuropsychiatric management of AD in clinics.

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Alzheimer’s Disease:Intracellular Beta Amyloid Completes the Irreversible Pathway from Spirochetes to Biofilms to Beta Amyloid to Hyperphosphorylated Tau Protein

Cited by 2 publications

References 14 publications

The Potential Role of Cytokines and Growth Factors in the Pathogenesis of Alzheimer’s Disease

The Potential Role of Cytokines and Growth Factors in the Pathogenesis of Alzheimer’s Disease

The Potential Role of Cytokines and Growth Factors in the Pathogenesis of Alzheimer’s Disease

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