Aβ plaques lead to aberrant regulation of calcium homeostasis in vivo resulting in structural and functional disruption of neuronal networks
Open accessAbstract
Alzheimer's disease is characterized by the deposition of senile plaques and progressive dementia. The molecular mechanisms that couple plaque deposition to neural system failure, however, are unknown. Using transgenic mouse models of AD together with multiphoton imaging, we measured neuronal calcium in individual neurites and spines in vivo using the genetically encoded calcium indicator Yellow Cameleon 3.6. Quantitative imaging revealed elevated [Ca(2+)]i (calcium overload) in approximately 20% of neurites in APP mice with cortical plaques, compared to less than 5% in wild-type mice, PS1 mutant mice, or young APP mice (animals without cortical plaques). Calcium overload depended on the existence and proximity to plaques. The downstream consequences included the loss of spinodendritic calcium compartmentalization (critical for synaptic integration) and a distortion of neuritic morphologies mediated, in part, by the phosphatase calcineurin. Together, these data demonstrate that senile plaques impair neuritic calcium homeostasis in vivo and result in the structural and functional disruption of neuronal networks.
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Aβ peptides in various forms have been linked to alterations in cerebral calcium homeostasis, axonal guidance, axonal transport, and/or synaptic signaling.
“A peptides in various forms have been linked to alterations in cerebral calcium homeostasis (Kuchibhotla et al., 2008), axonal guidance (Cao et al., 2012), axonal transport, and/or synaptic signaling (Knobloch et al., 2007a), processes that ultimately might translate into impaired neural function.”
From Early Alterations in Functional Connectivity and White Matter Structure in a Transgenic Mouse Model of Cerebral Amyloidosis (2014) · cites this paper as Kuchibhotla et al., 2008
Application of Aβ to hippocampal slices elevates resting Ca2+ levels.
“application of Aβ to hippocampal slices elevates resting Ca2+ levels [52, 53].”
From ApoE, ApoE Receptors, and the Synapse in Alzheimer's Disease (2017) · cites this paper as [53]
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Ca2+ Dyshomeostasis Disrupts Neuronal and Synaptic Function in Alzheimer’s Disease
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Self-citation
- Authors
- Kuchibhotla, K. V., Goldman, S. T., Lattarulo, C. R., Wu, H.-Y., Hyman, B. T., & Bacskai, B. J.
- Affiliations
- Harvard University (US)
- Massachusetts General Hospital (US)
- Corresponding author
- Bacskai, Brian J.
- Venue
- Neuron
- Publisher
- Elsevier BV
- Published
- 2008-07
- Volume
- 59
- Issue
- 2
- Pages
- 214-225
- ISSN
- 0896-6273 (ISSN-L)
- PMC
- PMC2578820
- OpenAlex
- W2023200476
- Cited by
- 614
- References
- 55
- Citations by year
- 2026: 21 · 2025: 20 · 2024: 40 · 2023: 31 · 2022: 33 · 2021: 49 · 2020: 34 · 2019: 30 · 2018: 40 · 2017: 28 · 2016: 27 · 2015: 32 · 2014: 33 · 2013: 38 · 2012: 34
- FWCI
- 28.07
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- www.elsevier.com/tdm/userlicense/1.0/ (tdm)
- www.elsevier.com/legal/tdmrep-license (tdm)
- www.elsevier.com/open-access/userlicense/1.0/ (vor, 1878 d)
- doi.org/10.15223/policy-017 (stm-asf)
- doi.org/10.15223/policy-037 (stm-asf)
- doi.org/10.15223/policy-012 (stm-asf)
- doi.org/10.15223/policy-029 (stm-asf)
- doi.org/10.15223/policy-004 (stm-asf)
- Locations
- Neuron (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health (AG08487, EB000768, NS580752)
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- Alzheimer's disease, amyloid plaques, amyloid-beta, calcium homeostasis, neurites, dendritic spines, calcium compartmentalization, calcineurin, neurite morphology, neuronal network dysfunction, APP transgenic mice
- MeSH terms
- Alzheimer Disease, Animals, Brain, Calcium, Cells, Cultured, Chickens, Cricetulus, Cricetinae, Homeostasis, Humans, Mice, Transgenic, Nerve Net, Neurons, Amyloid beta-Peptides, CHO Cells, Mice, Plaque, Amyloid
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