期刊
AGING CELL
卷 14, 期 1, 页码 122-129出版社
WILEY
DOI: 10.1111/acel.12281
关键词
Alzheimer's disease; amyloid-beta; ApoE genotype; CSF; leptin receptors; leptin
资金
- Swedish Brain Power
- Stockholm County Council
- Karolinska Institutet, Strategic Neuroscience Programme (Sweden)
- Margaretha af Ugglas Foundation (Sweden)
- Swedish Science Council
- Swedish Alzheimer's Foundation
- Gamla Tjanarinnor Foundation (Sweden)
- Gun och Bertil Stonhes Foundation (Sweden)
- Blanceflor Boncompagni-Ludovisi Foundation (Italy)
- Ramon Areces Foundation (Spain)
- AFA Soria (Spain)
- NIHR Biomedical Research Centre and Biomedical Research Unit for Dementia at South London
- Maudsley NHS Foundation Trust Alzheimer's Research UK
Several studies support the relation between leptin and Alzheimer's disease (AD). We show that leptin levels in CSF are unchanged as subjects progress to AD. However, in AD hippocampus, leptin signalling was decreased and leptin localization was shifted, being more abundant in reactive astrocytes and less in neurons. Similar translocation of leptin was found in brains from Tg2576 and apoE4 mice. Moreover, an enhancement of leptin receptors was found in hippocampus of young Tg2576 mice and in primary astrocytes and neurons treated with A(1-42). In contrast, old Tg2576 mice showed decreased leptin receptors levels. Similar findings to those seen in Tg2576 mice were found in apoE4, but not in apoE3 mice. These results suggest that leptin levels are intact, but leptin signalling is impaired in AD. Thus, A accumulation and apoE4 genotype result in a transient enhancement of leptin signalling that might lead to a leptin resistance state over time.
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