Journal
EMBO MOLECULAR MEDICINE
Volume 10, Issue 1, Pages 32-47Publisher
WILEY
DOI: 10.15252/emmm.201707825
Keywords
Alzheimer's disease; amyloid pathology; A beta channels; gene expression; membrane pores
Categories
Funding
- DZNE
- Max Planck Society
- Hans and Ilse Breuer Award for Alzheimer's disease
- DFG [FI981/9-1, SFB803]
- EU (ERC)
- Hans and Ilse Breuer Foundation
- CoEN Initiative [CoEN3018]
- Malta Council for Science AMP
- Technology through the National Research AMP
- Innovation Programme [RI-2008-068]
- University of Malta [PHBR06]
- Malta Government Scholarship Scheme
- National Institute on Aging of National Institutes of Health [AG028709]
- [SFB1089 C01]
- NATIONAL INSTITUTE ON AGING [R01AG028709] Funding Source: NIH RePORTER
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Alzheimer's disease is a devastating neurodegenerative disease eventually leading to dementia. An effective treatment does not yet exist. Here we show that oral application of the compound anle138b restores hippocampal synaptic and transcriptional plasticity as well as spatial memory in a mouse model for Alzheimer's disease, when given orally before or after the onset of pathology. At the mechanistic level, we provide evidence that anle138b blocks the activity of conducting Ab pores without changing the membrane embedded A beta-oligomer structure. In conclusion, our data suggest that anle138b is a novel and promising compound to treat AD-related pathology that should be investigated further.
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