蠻有趣的，應該是這篇文章 doi:10.1038/nature17172
Alzheimer’s disease (AD) is a neurodegenerative disorder characterized by
progressive memory decline and subsequent loss of broader cognitive
functions1. Memory decline in the early stages of AD is mostly limited to
episodic memory, for which the hippocampus has a crucial role2. However, it
has been uncertain whether the observed amnesia in the early stages of AD is
due to disrupted encoding and consolidation of episodic information, or an
impairment in the retrieval of stored memory information. Here we show that
in transgenic mouse models of early AD, direct optogenetic activation of
hippocampal memory engram cells results in memory retrieval despite the fact
that these mice are amnesic in long-term memory tests when natural recall
cues are used, revealing a retrieval, rather than a storage impairment.
Before amyloid plaque deposition, the amnesia in these mice is
age-dependent3, 4, 5, which correlates with a progressive reduction in spine
density of hippocampal dentate gyrus engram cells. We show that optogenetic
induction of long-term potentiation at perforant path synapses of dentate
gyrus engram cells restores both spine density and long-term memory. We also
demonstrate that an ablation of dentate gyrus engram cells containing
restored spine density prevents the rescue of long-term memory. Thus,
selective rescue of spine density in engram cells may lead to an effective
strategy for treating memory loss in the early stages of AD.
--
※ 發信站: 批踢踢實業坊(ptt.cc), 來自: 134.58.253.57
※ 文章網址: https://www.ptt.cc/bbs/Cognitive/M.1458581251.A.A03.html