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• W4226385215 endingPage "745" @default.
• W4226385215 startingPage "715" @default.
• W4226385215 abstract "Nearly 50 million people worldwide are suffering from age-related signs and symptoms of cognitive decline. Even after almost half a century from our first understanding of some of the neurobiological basis of AD, there are still no therapeutic approaches to prevent, delay, or reverse this disorder. At the onset, most patients show emotional and mild cognitive alterations that will advance to clear deficits in language, memory loss, and ultimately death. The cellular hallmarks of AD include intracellular neurofibrillary tangles and the extracellular deposition of senile plaques that are mainly made up of amyloid-β (Aβ1–42 and 1–40) peptides. Due to its physicochemical properties, Aβ can interact with the neuronal plasma membrane forming ion pores, and even rupturing the membrane, thus leading to cytoplasmic leakage and cell death. These disruptive effects of Aβ on the membrane might result from a direct interaction either with lipids or with proteins expressed in the membrane. As we will show in this review, there is abundant information indicating that membrane disruptions by misfolded proteins, like Aβ, might be associated to the presence of cholesterol. Cholesterol also affects the generation of Aβ and its cellular localization, thus affecting critical membrane proteins that regulate neuronal excitability and synaptic plasticity. Therefore, in the present review, we focus on the role of membrane cholesterol and its dysregulation in neurodegeneration, primarily in AD where the bulk of the published information is available." @default.
• W4226385215 created "2022-05-05" @default.
• W4226385215 creator A5002460435 @default.
• W4226385215 creator A5035423868 @default.
• W4226385215 creator A5046185483 @default.
• W4226385215 creator A5057319506 @default.
• W4226385215 date "2022-01-01" @default.
• W4226385215 modified "2023-09-26" @default.
• W4226385215 title "Involvement of cholesterol and β-amyloid in the initiation and progression of Alzheimer’s disease" @default.
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