What do we know about the long-term consequences of stress on ageing and the progression of age-related neurodegenerative disorders?

Pardon, Marie‐Christine; Rattray, Ivan

doi:10.1016/j.neubiorev.2008.03.005

Cited by 60 publications

(35 citation statements)

References 136 publications

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“…Stress-related genes increase with aging in the CNS, and a similar pattern has been observed for AD, suggesting that a continuum of increasing stress exists in the aging brain and that AD may represent the cumulative effects of such stress (Lukiw, 2004;Pardon and Rattray, 2008). There are reports of increased Hsp27 in AD brains and accumulation of HSPs in plaques, NFTs, and Lewy bodies (Stege et al, 1999;Smith et al, 2005;Wilhelmus et al, 2006b).…”

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confidence: 70%

The small heat shock protein Hsp27 protects cortical neurons against the toxic effects of β‐amyloid peptide

King

Nafar

Clarke

et al. 2009

J of Neuroscience Research

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Neurofibrillary tangles and amyloid plaques are considered to be hallmarks of Alzheimer's disease (AD), and the toxic effects of amyloid-beta peptide (A beta) lead to activation of stress-related signaling and neuronal loss. The small heat shock protein Hsp27 is reported to be increased in AD brains and to accumulate in plaques, but whether this represents a potentially protective response to stress or is part of the disease process is not known. We hypothesized that increased expression of Hsp27 in neurons can promote neuronal survival and stabilize the cytoskeleton in the face of A beta exposure. By using neonatal rat cortical neurons, we investigated the potential role of Hsp27 in neuronal cultures in the presence or absence of A beta. We initially tested whether a heat stress (HS) would be sufficient to induce endogenous Hsp27 expression. HS not only did not result in neuronal Hsp27 up-regulation but made the cells more vulnerable to A beta exposure. We then used cDNA transfection to overexpress EGFP-Hsp27 (or the empty vector) in cultures and then assessed neuronal survival and growth. Transfected neurons appeared healthy and had robust neuritic outgrowth. A beta treatment induced significant cell death by 48-72 hr in nontransfected and empty-vector-expressing cultures. In contrast, cultures expressing Hsp27 did not display significant apoptosis. Our results show that Hsp27-expressing neurons were selectively protected against the deleterious effects of A beta treatment; neuronal degeneration was prevented, and A beta-induced alterations in mitochondrial size were attenuated. We also demonstrate that Hsp27 expression can enhance neurite growth in cortical neurons compared with control vector-transfected cells. Overall, our study provides new evidence that Hsp27 can provide a protective influence in primary cortical neurons in the face of toxic concentrations of amyloid.

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confidence: 70%

The small heat shock protein Hsp27 protects cortical neurons against the toxic effects of β‐amyloid peptide

King

Nafar

Clarke

et al. 2009

J of Neuroscience Research

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“…The hippocampus, which is associated with cognition, is the most vulnerable region to aging and stress [42,43]. Aged animals show decreased plasma corticosterone levels [44], which downregulate glucocorticoid (GC) receptor synthesis and binding in the hippocampus and influence the function of the hypothalamo-pituitary-adrenal (HPA) axis, leading to a decrease in hippocampal neurons [43][44][45][46][47][48].…”

Section: Discussionmentioning

confidence: 99%

Effects of Chronic Stress on Cognition in Male SAMP8 Mice

Wang

Yuan²,

Pang³

et al. 2016

Cell Physiol Biochem

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Background/Aims: Chronic stress can lead to cognitive impairment. Senescence-accelerated mouse prone 8 (SAMP8) is a naturally occurring animal model that is useful for investigating the neurological mechanisms of Alzheimer's disease. Here we investigated the impact and mechanisms of chronic stress on cognition in male SAMP8 mice. Methods: Male 6-month- old SAMP8 and SAMR1 (senescence-accelerated mouse resistant 1) mice strains were randomly divided into 4 groups. Mice in the unpredictable chronic mild stress (UCMS) groups were exposed to diverse stressors for 4 weeks. Then, these mice performed Morris water maze (MWM) test to assess the effect of UCMS on learning and memory. To explore the neurological mechanisms of UCMS on cognition in mice, we evaluated changes in the expression of postsynaptic density 95 (PSD95) and synaptophysin (SYN), which are essential proteins for synaptic plasticity. Five mice from each group were randomly chosen for reverse transcription polymerase chain reaction (RT-PCR) and western blotting analysis of SYN and PSD95. Results: The Morris water maze experiment revealed that the cognitive ability of the SAMP8 mice decreased with brain aging, and that chronic stress aggravated this cognitive deficit. In addition, chronic stress decreased the mRNA and protein expression of SYN and PSD95 in the hippocampus of the SAMP8 mice; however, the SAMR1 mice were unaffected. Conclusion: Our results demonstrate that decreased cognition and synaptic plasticity are related to aging. Moreover, we show that chronic stress aggravated this cognitive deficit and decreased SYN and PSD95 expression in the SAMP8 mice. Furthermore, the SAMP8 mice were more vulnerable to the detrimental effects of chronic stress on cognition than the SAMR1 mice. Our results suggest that the neurological mechanisms of chronic stress on cognition might be associated with a decrease in hippocampal SYN and PSD95 expression, which is critical for structural synaptic plasticity.

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“…Vertebrate stress responses and ageing are closely inter-linked. Chronic stress is associated with increased exposure to oxidative and other damage and appears to accelerate the ageing process (Pardon and Rattray, 2008). In the case of the zebra finches in Fig.…”

Section: Reviewmentioning

confidence: 99%

Organismal stress, telomeres and life histories

Monaghan

2014

Journal of Experimental Biology

201

203

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Most organisms, including ourselves, are exposed to environmental stressors at various points during life, and responses to such stressors have been optimised by evolution to give the best fitness outcomes. It is expected that environmental change will substantially increase long-term stress exposure in many animal groups in the coming decades. A major challenge for biologists is to understand and predict how this will influence individuals, populations and ecosystems, and over what time scale such effects will occur. This requires a multi-disciplinary approach, combining studies of mechanisms with studies of fitness consequences for individuals and their descendants. In this review, I discuss the positive and negative fitness consequences of responses to stressful environments, particularly during early life, and with an emphasis on studies in birds. As many of the mechanisms underlying stress responses are highly conserved across the vertebrate groups, the findings from these studies have general applicability when interpreted in a life history context. One important route that has recently been identified whereby chronic stress exposure can affect health and longevity over long time frames is via effects on telomere dynamics. Much of this work has so far been done on humans, and is correlational in nature, but studies on other taxa, and experimental work, are increasing. I summarise the relevant aspects of vertebrate telomere biology and critically appraise our current knowledge with a view to pointing out important future research directions for our understanding of how stress exposure influences life histories.

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What do we know about the long-term consequences of stress on ageing and the progression of age-related neurodegenerative disorders?

Cited by 60 publications

References 136 publications

The small heat shock protein Hsp27 protects cortical neurons against the toxic effects of β‐amyloid peptide

The small heat shock protein Hsp27 protects cortical neurons against the toxic effects of β‐amyloid peptide

Effects of Chronic Stress on Cognition in Male SAMP8 Mice

Organismal stress, telomeres and life histories

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