ArticleActa neuropathologica2015
RCAN1 overexpression promotes age-dependent mitochondrial dysregulation related to neurodegeneration in Alzheimer's disease.
Article in Acta neuropathologica, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
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43 citing papers in PubMed, 91 citations in OpenAlex.
- PRMT5-Cacna1d axis maintains calcium homeostasis to regulate postnatal motor development in mice.Cellular and molecular life sciences : CMLS · 2026Article
- Promoting Research Excellence in Down Syndrome: Proceedings of the 5th International Conference of the Trisomy 21 Research Society.Neuromolecular medicine · 2026Article
- Exploring automated plasma phospho-tau217 assays for the diagnosis of Down syndrome-related Alzheimer's disease.Communications medicine · 2026Article
- Restoring RCAN1 dosage mitigates sleep and EEG abnormalities in a Down syndrome model.Neurobiology of disease · 2026Article
- Article
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- Troxerutin improves diabetic cognitive dysfunction by inhibiting mitochondrial fission mediated by transient receptor potential melastatin 7/calcineurin/dynamin-related protein 1World journal of diabetes · 2025Article
- Cargo of small extracellular vesicles from neuronal origin shows progression of dementia in individuals with Down syndrome.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Article
- Neuronal oscillations in cognition: Down syndrome as a model of mouse to human translation.The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry · 2025Review
- Mitochondrial Imbalance in Down Syndrome: A Driver of Accelerated Brain Aging?Aging and disease · 2025Review
- Article
- DSCR1 deficiency ameliorates the Aβ pathology of Alzheimer's disease by enhancing microglial activity.Life science alliance · 2023Article
- Senescent Microglia Represent a Subset of Disease-Associated Microglia in P301S Mice.Journal of Alzheimer's disease : JAD · 2023Article
- Targeting CaN/NFAT in Alzheimer's brain degeneration.Frontiers in immunology · 2023Review
- Consequences of chromosome gain: A new view on trisomy syndromes.American journal of human genetics · 2022Review
- Overexpression ofCells · 2022Article
- Targeting upregulated RNA binding protein RCAN1.1: a promising strategy for neuroprotection in acute ischemic stroke.CNS neuroscience & therapeutics · 2022Article
- Regulator of calcineurin 1 deletion attenuates mitochondrial dysfunction and apoptosis in acute kidney injury through JNK/Mff signaling pathway.Cell death & disease · 2022Article
- RCAN1 knockout and overexpression recapitulate an ensemble of rest-activity and circadian disruptions characteristic of Down syndrome, Alzheimer's disease, and normative aging.Journal of neurodevelopmental disorders · 2022Article
- APP and DYRK1A regulate axonal and synaptic vesicle protein networks and mediate Alzheimer's pathology in trisomy 21 neurons.Molecular psychiatry · 2022Article
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6 authors at 3 institutions in 1 country.
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Abstract
Aging is the largest risk factor for Alzheimer's disease (AD). Patients with Down syndrome (DS) develop symptoms consistent with early-onset AD, suggesting that overexpression of chromosome 21 genes such as Regulator of Calcineurin 1 (RCAN1) plays a role in AD pathogenesis. RCAN1 levels are increased in the brain of DS and AD patients but also in the human brain with normal aging. RCAN1 has been implicated in several neuronal functions, but whether its increased expression is correlative or causal in the aging-related progression of AD remains elusive. We show that brain-specific overexpression of the human RCAN1.1S isoform in mice promotes early age-dependent memory and synaptic plasticity deficits, tau pathology, and dysregulation of dynamin-related protein 1 (DRP1) activity associated with mitochondrial dysfunction and oxidative stress, reproducing key AD features. Based on these findings, we propose that chronic RCAN1 overexpression during aging alters DRP1-mediated mitochondrial fission and thus acts to promote AD-related progressive neurodegeneration.
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