Abstract
Diabetes is a risk factor for Alzheimer disease (AD). Apolipoprotein E (ApoE) and several genes related to AD have recently been identified by genome-wide association studies (GWAS) as being closely linked to lipid metabolism. Lipid metabolism and glucose-energy metabolism are closely related. Here, we review the emerging evidence regarding the roles of lipid and glucose metabolism in the modulation of β-amyloid, tau, and neurodegeneration during the pathogenesis of AD. Disruption of homeostasis of lipid and glucose metabolism affects production and clearance of β-amyloid and tau phosphorylation, and induces neurodegeneration. A more integrated understanding of the interactions among lipid, glucose, and protein metabolism is required to elucidate the pathogenesis of AD and to develop next-generation therapeutic options.
Highlights
INTRODUCTIONAlzheimer disease (AD) is a progressive neurodegenerative disorder that is pathologically characterized by cerebral atrophy ( within the hippocampus and temporal and parietal lobes), senile plaques, neurofibrillary tangles (NFT), and neuronal cell death
Alzheimer disease (AD) is a progressive neurodegenerative disorder that is pathologically characterized by cerebral atrophy, senile plaques, neurofibrillary tangles (NFT), and neuronal cell death
In addition to the Apolipoprotein E (ApoE) gene, recent genome-wide association studies (GWAS) have identified novel risk genes for AD (Hollingworth et al, 2011; Olgiati et al, 2011), and some of these genes are closely associated with lipid metabolism
Summary
Alzheimer disease (AD) is a progressive neurodegenerative disorder that is pathologically characterized by cerebral atrophy ( within the hippocampus and temporal and parietal lobes), senile plaques, neurofibrillary tangles (NFT), and neuronal cell death. Familial AD is caused by mutations in the amyloid precursor protein (Goate et al, 1991) and presenilin (Sherrington et al, 1995). These mutations cause overproduction of β-amyloid (Aβ), its longer form, Aβ42, which aggregates in vitro (Jarrett et al, 1993) and forms the initial deposits in the brain (Iwatsubo et al, 1994) to form senile plaques. We review the roles of lipid and glucose metabolism in modulating Aβ, tau, and neurodegeneration during the pathogenesis of AD (Table 1) and focus on novel therapy development
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