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RCAN1 overexpression promotes age-dependent mitochondrial dysregulation related to neurodegeneration in Alzheimer’s disease
Too much RCAN1 protein may cause age-related mitochondrial problems linked to brain cell loss in Alzheimer's disease
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Abstract
Brain-specific overexpression of the human RCAN1.1S isoform in mice promotes early age-dependent memory deficits and synaptic plasticity issues.
- Increased levels of RCAN1 are found in the brains of individuals with Down syndrome and Alzheimer's disease.
- RCAN1 expression is also elevated in the brains of normally aging humans.
- Overexpression of RCAN1.1S in mice leads to early deficits in memory and synaptic function.
- This overexpression is associated with tau pathology and altered activity of a protein involved in mitochondrial function.
- Chronic RCAN1 overexpression may disrupt mitochondrial fission processes, contributing to neurodegeneration linked to Alzheimer's disease.
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