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A case for a non‐transgenic animal model of Alzheimer's disease
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| Zeitschriftentitel: | Genes, Brain and Behavior |
|---|---|
| Personen und Körperschaften: | , |
| In: | Genes, Brain and Behavior, 4, 2005, 3, S. 157-172 |
| Format: | E-Article |
| Sprache: | Englisch |
| veröffentlicht: |
Wiley
|
| Schlagwörter: |
| author_facet |
Stéphan, A. Phillips, A. G. Stéphan, A. Phillips, A. G. |
|---|---|
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Stéphan, A. Phillips, A. G. |
| spellingShingle |
Stéphan, A. Phillips, A. G. Genes, Brain and Behavior A case for a non‐transgenic animal model of Alzheimer's disease Behavioral Neuroscience Neurology Genetics |
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stéphan, a. |
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Stéphan, A. Phillips, A. G. 1601-1848 1601-183X Wiley Behavioral Neuroscience Neurology Genetics http://dx.doi.org/10.1111/j.1601-183x.2004.00113.x <jats:p> <jats:bold>Alzheimer's disease (AD) is associated with an early impairment in memory and is the major cause of dementia in the elderly. β‐Amyloid (Aβ) is believed to be a primary factor in the pathogenic pathway leading to dementia. Mounting evidence suggests that this syndrome begins with subtle alterations in synaptic efficacy prior to extensive neuronal degeneration and that the synaptic dysfunction could be caused by diffusible oligomeric assemblies of Aβ. This paper reviews the findings from behavioral analysis, electrophysiology, neuropathology and nootropic drug screening studies involving exogenous administration of Aβ in normal rodent brains. This non‐transgenic model of amyloid pathology <jats:italic>in vivo</jats:italic> is presented as a complementary alternative model to transgenic mice to study the cellular and molecular pathways induced by amyloid, which in turn may be a causal factor in the disruption of cognition. The data reviewed here confirm that the diffusible form of Aβ rapidly induces synaptic dysfunction and a secondary process involving cellular cascades induced by the fibrillar form of amyloid. The time–course of alteration in memory processes implicates at least two different mechanisms that may be targeted with selective therapies aimed at improving memory in some AD patients.</jats:bold> </jats:p> A case for a non‐transgenic animal model of Alzheimer's disease Genes, Brain and Behavior |
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A case for a non‐transgenic animal model of Alzheimer's disease |
| title_unstemmed |
A case for a non‐transgenic animal model of Alzheimer's disease |
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A case for a non‐transgenic animal model of Alzheimer's disease |
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A case for a non‐transgenic animal model of Alzheimer's disease |
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A case for a non‐transgenic animal model of Alzheimer's disease |
| title_short |
A case for a non‐transgenic animal model of Alzheimer's disease |
| title_sort |
a case for a non‐transgenic animal model of alzheimer's disease |
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Behavioral Neuroscience Neurology Genetics |
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http://dx.doi.org/10.1111/j.1601-183x.2004.00113.x |
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2005 |
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157-172 |
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<jats:p> <jats:bold>Alzheimer's disease (AD) is associated with an early impairment in memory and is the major cause of dementia in the elderly. β‐Amyloid (Aβ) is believed to be a primary factor in the pathogenic pathway leading to dementia. Mounting evidence suggests that this syndrome begins with subtle alterations in synaptic efficacy prior to extensive neuronal degeneration and that the synaptic dysfunction could be caused by diffusible oligomeric assemblies of Aβ. This paper reviews the findings from behavioral analysis, electrophysiology, neuropathology and nootropic drug screening studies involving exogenous administration of Aβ in normal rodent brains. This non‐transgenic model of amyloid pathology <jats:italic>in vivo</jats:italic> is presented as a complementary alternative model to transgenic mice to study the cellular and molecular pathways induced by amyloid, which in turn may be a causal factor in the disruption of cognition. The data reviewed here confirm that the diffusible form of Aβ rapidly induces synaptic dysfunction and a secondary process involving cellular cascades induced by the fibrillar form of amyloid. The time–course of alteration in memory processes implicates at least two different mechanisms that may be targeted with selective therapies aimed at improving memory in some AD patients.</jats:bold> </jats:p> |
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| description | <jats:p> <jats:bold>Alzheimer's disease (AD) is associated with an early impairment in memory and is the major cause of dementia in the elderly. β‐Amyloid (Aβ) is believed to be a primary factor in the pathogenic pathway leading to dementia. Mounting evidence suggests that this syndrome begins with subtle alterations in synaptic efficacy prior to extensive neuronal degeneration and that the synaptic dysfunction could be caused by diffusible oligomeric assemblies of Aβ. This paper reviews the findings from behavioral analysis, electrophysiology, neuropathology and nootropic drug screening studies involving exogenous administration of Aβ in normal rodent brains. This non‐transgenic model of amyloid pathology <jats:italic>in vivo</jats:italic> is presented as a complementary alternative model to transgenic mice to study the cellular and molecular pathways induced by amyloid, which in turn may be a causal factor in the disruption of cognition. The data reviewed here confirm that the diffusible form of Aβ rapidly induces synaptic dysfunction and a secondary process involving cellular cascades induced by the fibrillar form of amyloid. The time–course of alteration in memory processes implicates at least two different mechanisms that may be targeted with selective therapies aimed at improving memory in some AD patients.</jats:bold> </jats:p> |
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| spelling | Stéphan, A. Phillips, A. G. 1601-1848 1601-183X Wiley Behavioral Neuroscience Neurology Genetics http://dx.doi.org/10.1111/j.1601-183x.2004.00113.x <jats:p> <jats:bold>Alzheimer's disease (AD) is associated with an early impairment in memory and is the major cause of dementia in the elderly. β‐Amyloid (Aβ) is believed to be a primary factor in the pathogenic pathway leading to dementia. Mounting evidence suggests that this syndrome begins with subtle alterations in synaptic efficacy prior to extensive neuronal degeneration and that the synaptic dysfunction could be caused by diffusible oligomeric assemblies of Aβ. This paper reviews the findings from behavioral analysis, electrophysiology, neuropathology and nootropic drug screening studies involving exogenous administration of Aβ in normal rodent brains. This non‐transgenic model of amyloid pathology <jats:italic>in vivo</jats:italic> is presented as a complementary alternative model to transgenic mice to study the cellular and molecular pathways induced by amyloid, which in turn may be a causal factor in the disruption of cognition. The data reviewed here confirm that the diffusible form of Aβ rapidly induces synaptic dysfunction and a secondary process involving cellular cascades induced by the fibrillar form of amyloid. The time–course of alteration in memory processes implicates at least two different mechanisms that may be targeted with selective therapies aimed at improving memory in some AD patients.</jats:bold> </jats:p> A case for a non‐transgenic animal model of Alzheimer's disease Genes, Brain and Behavior |
| spellingShingle | Stéphan, A., Phillips, A. G., Genes, Brain and Behavior, A case for a non‐transgenic animal model of Alzheimer's disease, Behavioral Neuroscience, Neurology, Genetics |
| title | A case for a non‐transgenic animal model of Alzheimer's disease |
| title_full | A case for a non‐transgenic animal model of Alzheimer's disease |
| title_fullStr | A case for a non‐transgenic animal model of Alzheimer's disease |
| title_full_unstemmed | A case for a non‐transgenic animal model of Alzheimer's disease |
| title_short | A case for a non‐transgenic animal model of Alzheimer's disease |
| title_sort | a case for a non‐transgenic animal model of alzheimer's disease |
| title_unstemmed | A case for a non‐transgenic animal model of Alzheimer's disease |
| topic | Behavioral Neuroscience, Neurology, Genetics |
| url | http://dx.doi.org/10.1111/j.1601-183x.2004.00113.x |