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Cited by 198

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Adverse Stress, Hippocampal Networks, and Alzheimer’s Disease

Open access
Rothman, Sarah M., Mattson, Mark P.·2010·NeuroMolecular Medicine

Abstract

Recent clinical data have implicated chronic adverse stress as a potential risk factor in the development of Alzheimer’s disease (AD) and data also suggest that normal, physiological stress responses may be impaired in AD. It is possible that pathology associated with AD causes aberrant responses to chronic stress, due to potential alterations in the hypothalamic–pituitary–adrenal (HPA) axis. Recent study in rodent models of AD suggests that chronic adverse stress exacerbates the cognitive deficits and hippocampal pathology that are present in the AD brain. This review summarizes recent findings obtained in experimental AD models regarding the influence of chronic adverse stress on the underlying cellular and molecular disease processes including the potential role of glucocorticoids. Emerging findings suggest that both AD and chronic adverse stress affect hippocampal neural networks in a similar fashion. We describe alterations in hippocampal plasticity, which occur in both chronic stress and AD including dendritic remodeling, neurogenesis, and long-term potentiation. Finally, we outline potential roles for oxidative stress and neurotrophic factor signaling as the key determinants of the impact of chronic stress on the plasticity of neural networks and AD pathogenesis.

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Metadata

Authors
Rothman, S. M., & Mattson, M. P.
Venue
NeuroMolecular Medicine
Published
2009-11-27
Volume
12
Issue
1
Pages
56-70
ISSN
  • 1535-1084 (ISSN-L)
  • 1559-1174
OpenAlex
W2089189148
Cited by
198
References
44
FWCI
4.47
Type
journal article
Language
en
Open access
green

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CoChat. (2026). Citation check: Adverse Stress, Hippocampal Networks, and Alzheimer’s Disease. https://app.cochat.ai/papers/10.1007/s12017-009-8107-9
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Rothman, S. M., & Mattson, M. P. (2010). Adverse Stress, Hippocampal Networks, and Alzheimer’s Disease. NeuroMolecular Medicine. https://doi.org/10.1007/s12017-009-8107-9

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