Abstract | INTRODUCTION: METHODS: Here we review use of YC3.6 in studying Alzheimer's disease using mouse models and discuss whether these studies support or refute the Calcium Hypothesis. RESULTS: YC3.6 studies showed that amyloidosis preceded dysfunction in neuronal calcium signaling and changes in synapse structure. This evidence supports the Calcium Hypothesis. DISCUSSION: In vivo YC3.6 studies point to calcium signaling as a promising therapeutic target; however, additional work is necessary to translate these findings to humans.
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Authors | Morgan R Miller, Yee Fun Lee, Ksenia V Kastanenka |
Journal | Alzheimer's & dementia : the journal of the Alzheimer's Association
(Alzheimers Dement)
Vol. 19
Issue 9
Pg. 4196-4203
(09 2023)
ISSN: 1552-5279 [Electronic] United States |
PMID | 37154246
(Publication Type: Journal Article, Review, Research Support, Non-U.S. Gov't, Research Support, N.I.H., Extramural)
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Copyright | © 2023 the Alzheimer's Association. |
Chemical References |
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Topics |
- Animals
- Mice
- Humans
- Alzheimer Disease
(metabolism)
- Calcium
(metabolism)
- Neurodegenerative Diseases
- Calcium Signaling
(physiology)
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