| Abstract No.: | 307 |
| Country: | Canada |
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| Title: | ALZHEIMER'S DISEASE |
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| Authors/Affiliations: | 1 Joanne McLaurin*;
1 University of Toronto, ON, Canada
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| Content: | Alzheimer’s disease is characterized by the accumulation of amyloid plaques, neurofibrillary tangles and neuronal loss. Although the initiation factor for sporadic AD has not been identified, the accumulation of the amyloid β-peptide (Aβ) initiates a cascade of events that leads to the formation of neurofibrillary tangles and neuronal loss. Transgenic mouse models of AD exhibit some but not all of these events. The over-expression and aggregation of Aβ initially causes neuronal synaptotoxicity, followed by axonal fibre loss and ultimately neuronal death. Soluble oligomers have been identified as the toxic species of Aβ and have been shown to induce tau hyperphosphorylation a prerequisite for the formation of neurofibrillary tangles. Therefore targeting oligomers may represent an effective therapeutic strategy to treat Alzheimer’s disease. When given orally cyclohexanehexol isomers inhibit aggregation of amyloid β-peptide (Aβ) in the brain and ameliorate AD-like phenotypes in the TgCRND8 mice, including impaired cognition, altered synaptic physiology, cerebral Aβ and accelerated mortality. These effects occur regardless of whether the compounds are given prior to, or well after the onset of the AD-like phenotype. |
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