Abstract
Alzheimer’s disease (AD) is a complex neurodegenerative disorder that leads to severe impairments in cognitive functions including memory and learning. An improved kinetic model is proposed here to understand the pathogenesis of AD in particular the role of glial cells in the presence of amyloid plaques and neurofibrillary tangles (NFTs). The kinetic model describes the production of activated microglia and astroglia. It involves two rate equations and incorporates the dual role of these glial cells which can function as neuroprotective and as neurotoxic cells. Examination of the steady state solutions of the model predicts an increase in population of these glial cells as (AD) progresses, and that this continues to increase linearly even after the amyloid population has reached a plateau.This is in agreement with experimental data. Limiting AD to the effect of amyloid peptides alone is incorrect and the role of neurofibrillary tangles, clearance rate of dead neurons and neuroinflammation from glial cells are vital and must be included in understanding the pathogenesis of AD. The study shows that increasing the clearance of dead neurons and use of any method to deactivate the glial cells will diminish the progression of AD.
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R. A. Thuraisingham is an honorary research fellow associated with the rehabilitation studies unit, Northern Clinical School University of Sydney, NSW 2065, Australia.
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Thuraisingham, R.A. A kinetic scheme to examine the role of glial cells in the pathogenesis of Alzheimer’s disease. Metab Brain Dis 37, 801–805 (2022). https://doi.org/10.1007/s11011-022-00902-z
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DOI: https://doi.org/10.1007/s11011-022-00902-z