Impaired learning and LTP in mice expressing the carboxy terminus of the Alzheimer amyloid precursor protein
Nature, ISSN: 0028-0836, Vol: 387, Issue: 6632, Page: 500-505
1997
- 317Citations
- 132Captures
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Example: if you select the 1-year option for an article published in 2019 and a metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019. If you select the 3-year option for the same article published in 2019 and the metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019, 2018 and 2017.
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Metrics Details
- Citations317
- Citation Indexes317
- 317
- CrossRef244
- Captures132
- Readers132
- 132
Article Description
Proteolytic processing of amyloid precursor protein (APP) through an endosomal/lysosomal pathway generates carboxyterminal polypeptides that contain an intact β-amyloid domain. Cleavage by as-yet unidentified proteases releases the β-amyloid peptide in soluble form. In Alzheimer's disease, aggregated β-amyloid is deposited in extracellular neuritic plaques. Although most of the molecular mechanisms involving β-amyloid and APP in the aetiology of Alzheimer's disease are still unclear, changes in APP metabolism may be important in the pathogenesis of the disease. Here we show that transgenic mice expressing the amyloidogenic carboxy-terminal 104 amino acids of APP develop, with ageing, extracellular β-amyloid immunoreactivity, increased gliosis and microglial reactivity, as well as cell loss in the CA1 region of the hippocampus. Adult transgenic mice demonstrate spatial-learning deficits in the Morris water maze and in maintenance of long-term potentiation (LTP). Our results indicate that alterations in the processing of APP may have considerable physiological effects on synaptic plasticity.
Bibliographic Details
Springer Science and Business Media LLC
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