ArticleNeuroscience letters2007
Aging is associated with elevated intracellular calcium levels and altered calcium homeostatic mechanisms in hippocampal neurons.
Article in Neuroscience letters, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
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Who cites it
48 citing papers in PubMed, 113 citations in OpenAlex.
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- GRPa-PRS: A risk stratification method to identify genetically-regulated pathways in polygenic diseases.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Article
- Neuronal Necroptosis Drives Neuroinflammation and Cognitive Decline Independent of Neuronal Cell Death.Aging and disease · 2025Article
- Target the Heart: A New Axis of Alzheimer's Disease Prevention.Journal of dementia and alzheimer's disease · 2025Article
- Selectively Blocking Small Conductance CaBiology · 2025Article
- Pathway analysis through mutual information.Bioinformatics (Oxford, England) · 2024Article
- An Improved Method for Growing Primary Neurons on Electron Microscopy Grids Co-Cultured with Astrocytes.International journal of molecular sciences · 2023Article
- Neuronal Senescence in the Aged Brain.Aging and disease · 2023Review
- Vimar/RAP1GDS1 promotes acceleration of brain aging after flies and mice reach middle age.Communications biology · 2023Article
- Distinct CSF biomarker-associated DNA methylation in Alzheimer's disease and cognitively normal subjects.Alzheimer's research & therapy · 2023Article
- Distinct CSF biomarker-associated DNA methylation in Alzheimer's disease and cognitively normal subjects.Research square · 2023Article
- Biomolecular Markers of Brain Aging.Advances in experimental medicine and biology · 2023Article
- Defective bone repletion in aged Balb/cBy mice was caused by impaired osteoblastic differentiation.Journal of bone and mineral metabolism · 2022Article
- Mechanisms of Acupuncture in Improving Alzheimer's Disease Caused by Mitochondrial Damage.Chinese journal of integrative medicine · 2022Review
- STIM and Orai Mediated Regulation of Calcium Signaling in Age-Related Diseases.Frontiers in aging · 2022Review
- The Molecular Basis for the Calcium-Dependent Slow Afterhyperpolarization in CA1 Hippocampal Pyramidal Neurons.Frontiers in physiology · 2021Review
- Age-related shift in LTD is dependent on neuronal adenosine AMolecular psychiatry · 2020Article
- Article
- Presenilin 1 increases association with synaptotagmin 1 during normal aging.Neurobiology of aging · 2020Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Aging is associated with increased vulnerability to neurodegenerative conditions such as Parkinson's and Alzheimer's disease and greater neuronal deficits after stroke and epilepsy. Emerging studies have implicated increased levels of intracellular calcium ([Ca(2+)](i)) for the neuronal loss associated with aging related disorders. Recent evidence demonstrates increased expression of voltage gated Ca(2+) channel proteins and associated Ca(2+) currents with aging. However, a direct comparison of [Ca(2+)](i) levels and Ca(2+) homeostatic mechanisms in hippocampal neurons acutely isolated from young and mid-age adult animals has not been performed. In this study, Fura-2 was used to determine [Ca(2+)](i) levels in CA1 hippocampal neurons acutely isolated from young (4-5 months) and mid-age (12-16 months) Sprague-Dawley rats. Our data provide the first direct demonstration that mid-age neurons in comparison to young neurons manifest significant elevations in basal [Ca(2+)](i) levels. Upon glutamate stimulation and a subsequent [Ca(2+)](i) load, mid-age neurons took longer to remove the excess [Ca(2+)](i) in comparison to young neurons, providing direct evidence that altered Ca(2+) homeostasis may be present in animals at significantly younger ages than those that are commonly considered aged (> or =24 months). These alterations in Ca(2+) dynamics may render aging neurons more vulnerable to neuronal death following stroke, seizures or head trauma. Elucidating the functionality of Ca(2+) homeostatic mechanisms may offer an understanding of the increased neuronal loss that occurs with aging, and allow for the development of novel therapeutic agents targeted towards decreasing [Ca(2+)](i) levels thereby restoring the systems that maintain normal Ca(2+) homeostasis in aged neurons.
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