Journal
NATURE
Volume 539, Issue 7628, Pages 187-196Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/nature20412
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Funding
- US National Institutes of Health [R01 NS051874, R01 NS078839, RF1 AG042978, RF1 AG047661]
- Barbara J. Weedon Fellowship
- Norman B. Leventhal Fellowship
- Human Frontier Science Program
- JPB Foundation
- Belfer Neurodegeneration Consortium
- Glenn Foundation for Medical Research
- Cure Alzheimer's Fund
- Alana Foundation
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Alzheimer's disease is a progressive loss of memory and cognition, for which there is no cure. Although genetic studies initially suggested a primary role for amyloid-beta in Alzheimer's disease, treatment strategies targeted at reducing amyloid-beta have failed to reverse cognitive symptoms. These clinical findings suggest that cognitive decline is the result of a complex pathophysiology and that targeting amyloid-beta alone may not be sufficient to treat Alzheimer's disease. Instead, a broad outlook on neural-circuit-damaging processes may yield insights into new therapeutic strategies for curing memory loss in the disease.
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