Insulin resistance, neuroinflammation, and Alzheimer's disease

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Journal titleReviews in the Neurosciences
Pages509525; # of pages: 17
Subjectamyloid; insulin; tau protein; amyloid precursor protein; age; Alzheimer disease; autophosphorylation; central nervous system; degenerative disease; drug targeting; insulin resistance; nerve degeneration; nervous system inflammation; neurofibrillary tangle; neurotoxicity; risk factor; inflammation; metabolism; signal transduction; Inflammation
AbstractAlzheimer's disease (AD) is the most common form of dementia. Pathologically, it is characterized by degeneration of neurons and synapses, the deposition of extracellular plaques consisting of aggregated amyloid-â (Aâ) peptides, and intracellular neurofibrillary tangles made up of hyperphosphorylated tau protein. Recently, the spotlights have been centered on two characteristics of AD, neuroinflammation and insulin resistance. Because both of these pathways play roles in synaptic dysfunction and neurodegeneration, they become potential targets for therapeutic intervention that could impede the progression of the disease. Here, we present an overview of the traditional amyloid hypothesis, as well as emerging data on both inflammatory and impaired insulin signaling pathways in AD. It becomes evident that more than one concurrent treatment can be synergistic and various combinations should be discussed as a potential therapeutic strategy to correct the anomalies in AD. Insulin resistance, Aâ/tau pathologies, neuroinflammation, and dysregulation of central nervous system homeostasis are intertwined processes that together create the complex pathology of AD and should be considered as a whole picture.
Publication date
Publisherde Gruyter
AffiliationNational Research Council Canada (NRC-CNRC); Human Health Therapeutics
Peer reviewedYes
NPARC number21275594
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Record identifier23e8fc3d-827e-4d6c-92ff-af42e8e9b868
Record created2015-07-14
Record modified2016-05-09
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