Abstract
Conflicting findings exist regarding the link between environmental factors and development of Alzheimer's disease (AD) in a variety of transgenic mouse models of AD. In the present study, we investigated the effect of behavioral stress on the onset and progression of Aβ pathology in the brains of TgCRND8 mice, a transgenic mouse model of AD. One group of TgCRND8 mice was subjected to restraint stress starting at 1 month of age until they were 3 months old, while restraint stress in the second group started at 4 months of age until they were 6 months old. After 2 months of treatment, no differences in the soluble, formic acid extracted, or histologically detected Aβ deposition in the cortical and hippocampal levels were found between non-stressed and stressed mice. These results showed that restraint stress alone failed to aggravate amyloid pathology when initiated either before or after the age of amyloid plaque deposition in TgCRND8 mice, suggesting that if stress aggravated AD phenotype, it may not be via an amyloid-related mechanism in the TgCRND8 mice. These findings are indicative that plaque load per se may not be used as a significant criterion for evaluating the effect of stress on AD patients.
Highlights
Alzheimer’s disease (AD), the most prevalent form of senile dementia, is characterized by two major histopathological hallmarks including Ab plaque and tau-laden neurofibrillary tangle formation [1]
Several genetic factors are known to be involved in early onset of familial AD [2,3,4,5,6], the etiology of sporadic AD that accounts for the majority of AD cases remains unclear [7;8]
Despite an intensive activation of the neurons of hypothalamic PVN and supraoptic nuclei (SON) and marked increased levels of corticosterone, the stress marker, under restraint stress, this treatment paradigm failed categorically to modify Ab pathology in the brains of TgCRND8 mice with treatment being initiated at the age of either 1 or 4 months
Summary
Alzheimer’s disease (AD), the most prevalent form of senile dementia, is characterized by two major histopathological hallmarks including Ab plaque and tau-laden neurofibrillary tangle formation [1]. Epidemiological studies suggest that AD can be modulated by environmental factors. Those who are prone to psychological distress are more likely to develop AD [9;10]. Studies have recently begun to investigate the effect of environmental factors on neuropathology and cognitive function in transgenic models of AD [13,14,15,16]. Environmental enrichment, such as increased physical activity, cognitive stimulation, or a combination of both, has been demonstrated to elicit different outcomes including a reduction [18,19,20,21], no effect [14;22;23], or even an exacerbation [24;25] in extracellular plaque pathology in animal models of AD
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
