Cyclohexanehexol inhibitors of Aβ aggregation prevent and reverse Alzheimer phenotype in a mouse model
JA McLaurin, ME Kierstead, ME Brown, CA Hawkes… - Nature medicine, 2006 - nature.com
JA McLaurin, ME Kierstead, ME Brown, CA Hawkes, MHL Lambermon, AL Phinney…
Nature medicine, 2006•nature.comWhen given orally to a transgenic mouse model of Alzheimer disease, cyclohexanehexol
stereoisomers inhibit aggregation of amyloid β peptide (Aβ) into high-molecular-weight
oligomers in the brain and ameliorate several Alzheimer disease–like phenotypes in these
mice, including impaired cognition, altered synaptic physiology, cerebral Aβ pathology and
accelerated mortality. These therapeutic effects, which occur regardless of whether the
compounds are given before or well after the onset of the Alzheimer disease–like …
stereoisomers inhibit aggregation of amyloid β peptide (Aβ) into high-molecular-weight
oligomers in the brain and ameliorate several Alzheimer disease–like phenotypes in these
mice, including impaired cognition, altered synaptic physiology, cerebral Aβ pathology and
accelerated mortality. These therapeutic effects, which occur regardless of whether the
compounds are given before or well after the onset of the Alzheimer disease–like …
Abstract
When given orally to a transgenic mouse model of Alzheimer disease, cyclohexanehexol stereoisomers inhibit aggregation of amyloid β peptide (Aβ) into high-molecular-weight oligomers in the brain and ameliorate several Alzheimer disease–like phenotypes in these mice, including impaired cognition, altered synaptic physiology, cerebral Aβ pathology and accelerated mortality. These therapeutic effects, which occur regardless of whether the compounds are given before or well after the onset of the Alzheimer disease–like phenotype, support the idea that the accumulation of Aβ oligomers has a central role in the pathogenesis of Alzheimer disease.
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