ArticleProceedings of the National Academy of Sciences of the United States of America1998
Calbindin D28k blocks the proapoptotic actions of mutant presenilin 1: reduced oxidative stress and preserved mitochondrial function.
Article in Proceedings of the National Academy of Sciences of the United States of America, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers, 1 of them a synthesis that pooled it.
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Who cites it
55 citing papers in PubMed, 1 synthesis or guideline pooled it, 219 citations in OpenAlex.
- Association between Antihypertensive Drug Use and the Incidence of Cognitive Decline and Dementia: A Meta-Analysis of Prospective Cohort Studies.BioMed research international · 2017Pooled it
- Inflammatory mechanisms underlying early Alzheimer's disease pathology: evidence from the aging rhesus macaque brain.Frontiers in cellular neuroscience · 2026Review
- Scientific rationale for the use of α2A-adrenoceptor agonists in treating neuroinflammatory cognitive disorders.Molecular psychiatry · 2023Review
- Expression of the Calcium-Binding Protein CALB1 Is Induced and Controls Intracellular CaInternational journal of molecular sciences · 2022Article
- Design and Experimental Evaluation of a Peptide Antagonist against Amyloid β(1-42) Interactions with Calmodulin and Calbindin-D28k.International journal of molecular sciences · 2022Article
- Mitochondrial Dysfunction in Alzheimer's Disease: A Biomarker of the Future?Biomedicines · 2021Review
- Mechanism ofEvidence-based complementary and alternative medicine : eCAM · 2021Article
- Metabolic regulation of aging and age-related disease.Ageing research reviews · 2020Review
- Protective effects of calbindin‑D28K on the UVB radiation‑induced apoptosis of human lens epithelial cells.International journal of molecular medicine · 2020Article
- Intracellular Calcium Dysregulation by the Alzheimer's Disease-Linked Protein Presenilin 2.International journal of molecular sciences · 2020Review
- Posterior basolateral amygdala to ventral hippocampal CA1 drives approach behaviour to exert an anxiolytic effect.Nature communications · 2020Article
- Isx9 Regulates Calbindin D28K Expression in Pancreatic β Cells and Promotes β Cell Survival and Function.International journal of molecular sciences · 2018Article
- Towards a circuit-level understanding of hippocampal CA1 dysfunction in Alzheimer's disease across anatomical axes.Journal of Alzheimer's disease & Parkinsonism · 2018Article
- Neuroprotective effects of ischemic preconditioning on hippocampal CA1 pyramidal neurons through maintaining calbindin D28k immunoreactivity following subsequent transient cerebral ischemia.Neural regeneration research · 2017Article
- Identification of novel regulatory NFAT and TFII-I binding elements in the calbindin-D28k promoter in response to serum deprivation.Biochemical and biophysical research communications · 2015Article
- Neuronal amyloid-β accumulation within cholinergic basal forebrain in ageing and Alzheimer's disease.Brain : a journal of neurology · 2015Article
- Crucial role of calbindin-D28k in the pathogenesis of Alzheimer's disease mouse model.Cell death and differentiation · 2014Article
- Effect of Androsterone after Pilocarpine-induced Status Epilepticus in Mice.Journal of epilepsy research · 2014Article
- Focal cerebral ischemic injury decreases calbindin expression in brain tissue and HT22 cells.Laboratory animal research · 2013Article
- Effects of diphenyl diselenide on methylmercury toxicity in rats.BioMed research international · 2013Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Mutations in the presenilin 1 (PS-1) gene account for many cases of early-onset autosomal dominant inherited forms of Alzheimer's disease. Recent findings suggest that PS-1 mutations may sensitize neurons to apoptosis induced by trophic factor withdrawal and exposure to amyloid beta-peptide (Abeta). We now report that overexpression of the calcium-binding protein calbindin D28k prevents apoptosis in cultured neural cells expressing mutant PS-1 (L286V and M146V missense mutations). Elevations of the intracellular Ca2+ concentration and generation of reactive oxygen species induced by Abeta, and potentiated by mutant PS-1, were suppressed in calbindin-overexpressing cells. Impairment of mitochondrial function by Abeta (which preceded apoptosis) was exacerbated by PS-1 mutations and was largely prevented by calbindin. These findings suggest that PS-1 mutations render neurons vulnerable to apoptosis by a mechanism involving destabilization of cellular calcium homeostasis, which leads to oxidative stress and mitochondrial dysfunction.
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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.