Alzheimer’s disease (AD) and type 2 diabetes mellitus (T2DM) are two progressive and devastating health
disorders afflicting millions of people worldwide. The probability and incidence of both have increased considerably in
recent years consequent to increased longevity and population growth. Progressively more links are being continuously
found between inflammation and central nervous system disorders like AD, Parkinson's disease, Huntington's disease,
motor neuron disease, multiple sclerosis, stroke, traumatic brain injury and even cancers of the nervous tissue. The depth
of the relationship depends on the timing and extent of anti- or pro-inflammatory gene expression. Inflammation has also
been implicated in T2DM. Misfolding and fibrillization (of tissue specific and/or non-specific proteins) are features
common to both AD and T2DM and are induced by as well as contribute to inflammation and stress (oxidative/
glycation). This review appraises the roles of inflammation and abnormalities in the insulin signaling system as important
shared features of T2DM and AD. The capacity of anti-cholinesterases in reducing the level of certain common
inflammatory markers in particular if they may provide therapeutic potential to mitigate awry mechanisms leading to AD.
Keywords: Alzheimer’s disease, Anti-cholinesterase, Butyrylcholinesterase, Inflammation, Type 2 diabetes mellitus.
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