ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2011
Do RCAN1 proteins link chronic stress with neurodegeneration?
Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 46 citations in OpenAlex.
- Mitochondrial Imbalance in Down Syndrome: A Driver of Accelerated Brain Aging?Aging and disease · 2025Review
- Targeting ferroptosis for neuroprotection: potential therapeutic avenues in neurodegenerative and neuropsychiatric diseases.Frontiers in physiology · 2025Review
- Review
- Proteomic and metabolomic profiling of acute and chronic stress events associated with military exercises.Molecular omics · 2022Article
- RCAN1.4 attenuates renal fibrosis through inhibiting calcineurin-mediated nuclear translocation of NFAT2.Cell death discovery · 2021Article
- Protective Effect of Hydroxysafflor Yellow A against Chronic Mild Stress-induced Memory Impairments by Suppressing Tau Phosphorylation in Mice.Current medical science · 2021Article
- Identification of new BACE1 inhibitors for treating Alzheimer's disease.Journal of molecular modeling · 2021Article
- Signalling Pathways Implicated in Alzheimer's Disease Neurodegeneration in Individuals with and without Down Syndrome.International journal of molecular sciences · 2020Review
- RCAN1 Inhibits BACE2 Turnover by Attenuating Proteasome-Mediated BACE2 Degradation.BioMed research international · 2020Article
- Article
- The role of declining adaptive homeostasis in ageing.The Journal of physiology · 2017Review
- The Proteasome and Oxidative Stress in Alzheimer's Disease.Antioxidants & redox signaling · 2016Review
- The calcineurin inhibitor Sarah (Nebula) exacerbates Aβ42 phenotypes in a Drosophila model of Alzheimer's disease.Disease models & mechanisms · 2016Article
- RCAN1 overexpression promotes age-dependent mitochondrial dysregulation related to neurodegeneration in Alzheimer's disease.Acta neuropathologica · 2015Article
- Aberrant expression of RCAN1 in Alzheimer's pathogenesis: a new molecular mechanism and a novel drug target.Molecular neurobiology · 2014Review
- Overexpression of Rcan1-1L inhibits hypoxia-induced cell apoptosis through induction of mitophagy.Molecules and cells · 2014Article
- Impact of offspring death on cognitive health in late life: the Cache County study.The American journal of geriatric psychiatry : official journal of the American Association for Geriatric Psychiatry · 2014Article
- Neuropathological role of PI3K/Akt/mTOR axis in Down syndrome brain.Biochimica et biophysica acta · 2014Article
- Article
- RCAN1 regulates mitochondrial function and increases susceptibility to oxidative stress in mammalian cells.Oxidative medicine and cellular longevity · 2014Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 3 countries.
Funding
Abstract
It has long been suspected that chronic stress can exacerbate, or even cause, disease. We now propose that the RCAN1 gene, which can generate several RCAN1 protein isoforms, may be at least partially responsible for this phenomenon. We review data showing that RCAN1 proteins can be induced by multiple stresses, and present new data also implicating psychosocial/emotional stress in RCAN1 induction. We further show that transgenic mice overexpressing the RCAN1-1L protein exhibit accumulation of hyperphosphorylated tau protein (AT8 antibody), an early precursor to the formation of neurofibrillary tangles and neurodegeneration of the kind seen in Alzheimer disease. We propose that, although transient induction of the RCAN1 gene might protect cells against acute stress, persistent stress may cause chronic RCAN1 overexpression, resulting in serious side effects. Chronically elevated levels of RCAN1 proteins may promote or exacerbate various diseases, including tauopathies such as Alzheimer disease. We propose that the mechanism by which stress can lead to these diseases involves the inhibition of calcineurin and the induction of GSK-3β by RCAN1 proteins. Both inhibition of calcineurin and induction of GSK-3β contribute to accumulation of phosphorylated tau, formation of neurofibrillary tangles, and eventual neurodegeneration.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.