期刊
NEURON
卷 107, 期 6, 页码 1095-+出版社
CELL PRESS
DOI: 10.1016/j.neuron.2020.06.023
关键词
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资金
- NIH [R01AG063864, R01AG066806]
- BrightFocus Foundation [A2019380S]
- Alzheimer's Association [AARG-17-532932]
- Brain Research Foundation [BRFSG-2017-04]
- Donors Cure Foundation [CCAD201902]
- Japan Science and Technology Agency [JPMJPR1681]
- Whitehall Foundation [2017-08-01]
- RIKEN
- Ministry of Education, Culture, Sports, Science, and Technology (MEXT)
- Ministry of Health and Welfare
- Japan Agency for Medical Research and Development (AMED) [JP18dm0207001]
- University of California, Irvine Medical Scientist Training Program (MSTP) [NIH T32GM008620]
- NATIONAL INSTITUTE ON AGING [F31AG069500] Funding Source: NIH RePORTER
Patients with Alzheimer's disease (AD) suffer from spatial memory impairment and wandering behavior, but the brain circuit mechanisms causing such symptoms remain largely unclear. In healthy brains, spatially tuned hippocampal place cells and entorhinal grid cells exhibit distinct spike patterns in different environments, a circuit function called remapping.'' We tested remapping in amyloid precursor protein knockin (APP-KI) mice with impaired spatial memory. CA1 neurons, including place cells, showed disrupted remapping, although their spatial tuning was only mildly diminished. Medial entorhinal cortex (MEC) neurons severely lost their spatial tuning and grid cells were almost absent. Fast gamma oscillatory coupling between the MEC and CA1 was also impaired. Mild disruption of MEC grid cells emerged in younger APP-KI mice, although the spatial memory and CA1 remapping of the animals remained intact. These results point to remapping impairment in the hippocampus, possibly linked to grid cell disruption, as circuit mechanisms underlying spatial memory impairment in AD.
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