Pathogenic mechanisms of Alzheimer's disease analyzed in the APP23 transgenic mouse model.
作者： CHRISTINE STURCHLER-PIERRAT , MATTHIAS STAUFENBIEL
DOI: 10.1111/J.1749-6632.2000.TB06915.X
关键词:
摘要: APP23 transgenic mice overexpress human APP with the Swedish double mutation. The start to develop amyloid plaque pathology at about six months of age, followed somewhat later by vascular deposits. Plaques are mostly compact type and increase exponentially during aging. Female show a slightly more rapid A beta deposition than do male animals. Associated inflammatory reactions, neuritic synaptic degeneration as well tau hyperphosphorylation. Older have reduced cholinergic fiber length neuron number in hippocampal CA1 region. Crossbreeding expressing presenilin 1 carrying Alzheimer's disease-linked mutations lead an enhancement pathology. line is suitable model analyze contribution APP, beta, pathogenesis disease.
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