Spines, Plasticity, and Cognition in Alzheimer's Model Mice
The pathological hallmarks of Alzheimer's disease (AD)—widespread synaptic and neuronal loss and the pathological accumulation of amyloid-beta peptide (Aβ) in senile plaques, as well as hyperphosphorylated tau in neurofibrillary tangles—have been known for many decades, but the links between AD...
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| Format: | Article |
| Language: | English |
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Wiley
2012-01-01
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| Series: | Neural Plasticity |
| Online Access: | http://dx.doi.org/10.1155/2012/319836 |
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| author | Tara Spires-Jones Shira Knafo |
| author_facet | Tara Spires-Jones Shira Knafo |
| author_sort | Tara Spires-Jones |
| collection | DOAJ |
| description | The pathological hallmarks of Alzheimer's disease (AD)—widespread synaptic and neuronal loss and the pathological accumulation of amyloid-beta peptide (Aβ) in senile plaques, as well as hyperphosphorylated tau in neurofibrillary tangles—have been known for many decades, but the links between AD pathology and dementia and effective therapeutic strategies remain elusive. Transgenic mice have been developed based on rare familial forms of AD and frontotemporal dementia, allowing investigators to test in detail the structural, functional, and behavioral consequences of AD-associated pathology. Here, we review work on transgenic AD models that investigate the degeneration of dendritic spine structure, synaptic function, and cognition. Together, these data support a model of AD pathogenesis in which soluble Aβ initiates synaptic dysfunction and loss, as well as pathological changes in tau, which contribute to both synaptic and neuronal loss. These changes in synapse structure and function as well as frank synapse and neuronal loss contribute to the neural system dysfunction which causes cognitive deficits. Understanding the underpinnings of dementia in AD will be essential to develop and evaluate therapeutic approaches for this widespread and devastating disease. |
| format | Article |
| id | doaj-art-db535c05e6d246a78b0aa15f0068c574 |
| institution | Kabale University |
| issn | 2090-5904 1687-5443 |
| language | English |
| publishDate | 2012-01-01 |
| publisher | Wiley |
| record_format | Article |
| series | Neural Plasticity |
| spelling | doaj-art-db535c05e6d246a78b0aa15f0068c5742025-02-03T01:10:34ZengWileyNeural Plasticity2090-59041687-54432012-01-01201210.1155/2012/319836319836Spines, Plasticity, and Cognition in Alzheimer's Model MiceTara Spires-Jones0Shira Knafo1Massachusetts General Hospital, Harvard Medical School, 114 16th Street, Charlestown, MA 02129, USACentro de Biología Molecular “Severo Ochoa,” Consejo Superior de Investigaciones Científicas (CSIC) and Universidad Autónoma de Madrid, Nicolás Cabrera, 28049 Madrid, SpainThe pathological hallmarks of Alzheimer's disease (AD)—widespread synaptic and neuronal loss and the pathological accumulation of amyloid-beta peptide (Aβ) in senile plaques, as well as hyperphosphorylated tau in neurofibrillary tangles—have been known for many decades, but the links between AD pathology and dementia and effective therapeutic strategies remain elusive. Transgenic mice have been developed based on rare familial forms of AD and frontotemporal dementia, allowing investigators to test in detail the structural, functional, and behavioral consequences of AD-associated pathology. Here, we review work on transgenic AD models that investigate the degeneration of dendritic spine structure, synaptic function, and cognition. Together, these data support a model of AD pathogenesis in which soluble Aβ initiates synaptic dysfunction and loss, as well as pathological changes in tau, which contribute to both synaptic and neuronal loss. These changes in synapse structure and function as well as frank synapse and neuronal loss contribute to the neural system dysfunction which causes cognitive deficits. Understanding the underpinnings of dementia in AD will be essential to develop and evaluate therapeutic approaches for this widespread and devastating disease.http://dx.doi.org/10.1155/2012/319836 |
| spellingShingle | Tara Spires-Jones Shira Knafo Spines, Plasticity, and Cognition in Alzheimer's Model Mice Neural Plasticity |
| title | Spines, Plasticity, and Cognition in Alzheimer's Model Mice |
| title_full | Spines, Plasticity, and Cognition in Alzheimer's Model Mice |
| title_fullStr | Spines, Plasticity, and Cognition in Alzheimer's Model Mice |
| title_full_unstemmed | Spines, Plasticity, and Cognition in Alzheimer's Model Mice |
| title_short | Spines, Plasticity, and Cognition in Alzheimer's Model Mice |
| title_sort | spines plasticity and cognition in alzheimer s model mice |
| url | http://dx.doi.org/10.1155/2012/319836 |
| work_keys_str_mv | AT taraspiresjones spinesplasticityandcognitioninalzheimersmodelmice AT shiraknafo spinesplasticityandcognitioninalzheimersmodelmice |