Too much RCAN1 protein may cause age-related mitochondrial problems linked to brain cell loss in Alzheimer's disease

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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