ReviewAIMS neuroscience2019
Alzheimer's Disease: A short introduction to the calmodulin hypothesis.
Review in AIMS neuroscience, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 20 citations in OpenAlex.
- A Genome-wide Association Study of Alzheimer's Disease and Dementia in a Large Multi-ancestry Military Cohort Identifies Many New Dementia-Associated Loci.medRxiv : the preprint server for health sciences · 2026Article
- Role of tRNA-Derived Fragments and Their Modifications in the Pathogenesis and Treatment of Alzheimer's Disease.Molecular neurobiology · 2025Review
- Fabrication of a polymer brush-functionalized porphyrin-based covalent organic framework for enrichment of N-glycopeptides.Mikrochimica acta · 2023Article
- The Protective Effect of Mangiferin on Formaldehyde-Induced HT22 Cell Damage and Cognitive Impairment.Pharmaceutics · 2023Article
- Calmodulin Binding Domains in Critical Risk Proteins Involved in Neurodegeneration.Current issues in molecular biology · 2022Article
- Calmodulin binding proteins and neuroinflammation in multiple neurodegenerative diseases.BMC neuroscience · 2022Review
- Effects of Specific Inhibitors for CaMK1D on a Primary Neuron Model for Alzheimer's Disease.Molecules (Basel, Switzerland) · 2021Article
- Immune System and Neuroinflammation in Idiopathic Parkinson's Disease: Association Analysis of Genetic Variants and miRNAs Interactions.Frontiers in genetics · 2021Article
- Genetic Determinants Highlight the Existence of Shared Etiopathogenetic Mechanisms Characterizing Age-Related Macular Degeneration and Neurodegenerative Disorders.Frontiers in neurology · 2021Article
- Calmodulin Binding Proteins and Alzheimer's Disease: Biomarkers, Regulatory Enzymes and Receptors That Are Regulated by Calmodulin.International journal of molecular sciences · 2020Review
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
At the cellular level, Alzheimer's disease (AD) is characterized by the presence of intracellular plaques containing amyloid beta (Aβ) protein and neurofibrillary tangles consisting of phospho-tau (p-tau). These biomarkers are considered to contribute, at least in part, to the neurodegenerative events of the disease. But the accumulation of plaques and tangles is widely considered to be a later event with other factors likely being the cause of the disease. Calcium dysregulation-the unregulated accumulation of calcium ions-in neurons is an early event that underlies neurodegeneration. In 2002, O'Day and Myre extended this "Calcium Hypothesis" to include calmodulin (CaM) the primary target of calcium, suggesting the "Calmodulin Hypothesis" as an updated alternative. Here we overview the central role of CaM in the formation of the classic hallmarks of AD: plaques and tangles. Then some insight into CaM's binding to various risk factor proteins is given followed by a short summary of specific receptors and channels linked to the disease that are CaM binding proteins. Overall, this review emphasizes the diversity of Alzheimer's-linked CaM-binding proteins validating the hypothesis that CaM operates critically at all stages of the disease and stands out as a potential primary target for future research.
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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.