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NATURE
[2] Neuroscience: Restoring memory recall in mice with early
Alzheimer’s (N&V) *IMAGES*
The loss of episodic memories in the early stages of Alzheimer’s disease (AD) results from
impaired retrieval, rather than encoding, of information, reports a paper published online this
week in Nature. The study, conducted in mouse models of early AD, demonstrates that forgotten
memories can be rescued by directly activating specific cells in the hippocampus.
Several studies have suggested that the inability to remember an event (episodic memory)
observed in AD patients is a result of ineffective encoding of new information. However, because
cognitive tests rely on memory retrieval, it has been unclear whether it is poor encoding or poor
retrieval of information that contributes to memory impairments.
Susumu Tonegawa and colleagues address this question by studying three different types of
transgenic mice, which are amnesic and fail long-term memory tests. They find that
optogenetically stimulating hippocampal dentate gyrus engram cells leads to the restoration of
memory in early AD mice, such that they perform as well as control mice in a contextual fearconditioning task. The authors report that spine density of dentate gyrus engram cells is
correlated with amnesia in early AD and that without these cells, the rescue of long-term memory
is not possible. They note that further research is needed to determine whether the long-term
maintenance of memory storage declines as the disease progresses and to examine the
mechanisms underlying cognitive impairments in non-episodic memory.
ARTICLE DETAILS
DOI: 10.1038/nature17172
Corresponding Author:
Susumu Tonegawa
Massachusetts Institute of Technology, Cambridge, Massachusetts, United States
Email: tonegawa@mit.edu Tel: +1 617 253 6459
N&V Author
Eric Klann
New York University, New York, NY, USA
Email: ek65@nyu.edu
Please link to the article in online versions of your report (the URL will go live after the embargo ends):
http://nature.com/articles/doi:10.1038/nature17172
Image 1
Caption: This image represents a coronal brain section from a mouse model of early Alzheimer’s disease (AD).
These AD mice exhibit severe β-amyloid plaques (green) in the cortex and hippocampus at 9-months of age.
Credit: Dheeraj Roy
Copyright holder email: d_roy@mit.edu and tonegawa@mit.edu
Image 2
Caption: This image represents a coronal section of hippocampal dentate gyrus (DG) from a mouse model of
early Alzheimer’s disease. These AD mice lack β-amyloid plaques at 7-months of age. Using these mice
combined with a novel viral strategy, memory engram cells (green) for a contextual fear memory were tagged
with a light-sensitive protein channelrhodopsin-2.
Credit: Dheeraj Roy
Copyright holder email: d_roy@mit.edu and tonegawa@mit.edu
Image 3
Caption: This image represents a coronal section of hippocampal dentate gyrus (DG) from a mouse model of
early Alzheimer’s disease (AD). These AD mice exhibit severe β-amyloid plaques (red) in the DG at 9 months of
age. Using these mice combined with a novel viral strategy, memory engram cells (green) for a contextual fear
memory were tagged with a light-sensitive protein channelrhodopsin-2.
Credit: Dheeraj Roy
Copyright holder email: d_roy@mit.edu and tonegawa@mit.edu
Image 4
Caption: This image depicts a single memory engram cell (green) in the hippocampal dentate gyrus (DG) region
of a mouse model of early Alzheimer’s disease. To optically manipulate specific connections to these engram
cells, a blue light-sensitive protein oChIEF was expressed in an upstream brain region, i.e. medial entorhinal
cortical (EC) inputs (red) to the DG. The majority of DG granule cells were not active during memory engram
tagging (blue, non-engram cells).
Credit: Dheeraj Roy
Copyright holder email: d_roy@mit.edu and tonegawa@mit.edu