Oxidative stress in Alzheimer's disease hippocampus: A topographical study

Cruz-Sánchez, F. F.; Gironès, Xavier; Ortega, Arantxa; Alameda, Francesc; Lafuente, José Vicente

doi:10.1016/j.jns.2010.08.029

Cited by 40 publications

(30 citation statements)

References 16 publications

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“…Another study found CSF and blood serum concentrations of pentosidine cross-sectionally related to vascular dementia. 19 AGEs colocalize with several AD-related proteins, including tau proteins, ␤-amyloid (A␤), [5][6][7][8]10,20 and APOE. 9 As a result, pentosidine and other AGEs are prominent neuropathic features of plaques and NFTs and correlate with the progression of senile plaques in AD brains.…”

Section: Resultsmentioning

confidence: 99%

Advanced glycation end product level, diabetes, and accelerated cognitive aging

Yaffe¹,

Lindquist²,

Schwartz³

et al. 2011

Neurology

129

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Objective: Several studies report that diabetes increases risk of cognitive impairment; some have hypothesized that advanced glycation end products (AGEs) underlie this association. AGEs are cross-linked products that result from reactions between glucose and proteins. Little is known about the association between peripheral AGE concentration and cognitive aging. Methods:We prospectively studied 920 elders without dementia, 495 with diabetes and 425 with normal glucose (mean age 74.0 years). Using mixed models, we examined baseline AGE concentration, measured with urine pentosidine and analyzed as tertile, and performance on the Modified Mini-Mental State Examination (3MS) and Digit Symbol Substitution Test (DSST) at baseline and repeatedly over 9 years. Incident cognitive impairment (a decline of Ͼ1.0 SD on each test) was analyzed with logistic regression.Results: Older adults with high pentosidine level had worse baseline DSST score (p ϭ 0.05) but not different 3MS score (p ϭ 0.32). On both tests, there was a more pronounced 9-year decline in those with high and mid pentosidine level compared to those in the lowest tertile (3MS 7.0, 5.4, and 2.5 point decline, p overall Ͻ0.001; DSST 5.9, 7.4, and 4.5 point decline, p ϭ 0.03). Incident cognitive impairment was higher in those with high or mid pentosidine level than those in the lowest tertile (3MS: 24% vs 17%, odds ratio ϭ 1.55; 95% confidence interval 1.07-2.26; DSST: 31% vs 22%, odds ratio ϭ 1.62; 95% confidence interval 1.13-2.33). There was no interaction between pentosidine level, diabetes status, and cognitive decline. Multivariate adjustment for age, sex, race, education, hypertension, cardiovascular disease, estimated glomerular filtration rate, and diabetes diminished results somewhat but overall patterns remained similar. Conclusion:High peripheral AGE level is associated with greater cognitive decline in older adults with and without diabetes. Neurology ® 2011;77:1351-1356 GLOSSARY 3MS ϭ Modified Mini-Mental State Examination; A␤ ϭ ␤-amyloid; AD ϭ Alzheimer disease; ADA ϭ American Diabetes Association; AGE ϭ advanced glycation end product; BMI ϭ body mass index; CES-D ϭ Center for Epidemiologic Studies-Depression Scale; CI ϭ confidence interval; CV ϭ coefficient of variation; DSST ϭ Digit Symbol Substitution Test; eGFR ϭ estimated glomerular filtration rate; Health ABC ϭ Health, Aging and Body Composition; MDRD ϭ Modification of Diet in Renal Disease; NFT ϭ neurofibrillary tangle; OR ϭ odds ratio; RAGE ϭ receptor for advanced glycation end product; SE ϭ standard error.Mounting evidence suggests that diabetes increases risk for cognitive impairment and dementia, including Alzheimer disease (AD), 1 although the pathogenesis is unknown. Accumulation of advanced glycation end products (AGEs) in the brain is one possible mechanism linking diabetes to cognitive impairment. AGEs are a group of highly stable crosslinked products that form through a series of reactions between glucose and proteins. While AGEs form during normal aging, formation accele...

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Section: Resultsmentioning

confidence: 99%

Advanced glycation end product level, diabetes, and accelerated cognitive aging

Yaffe¹,

Lindquist²,

Schwartz³

et al. 2011

Neurology

129

View full text Add to dashboard Cite

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“…Evidence for activation of the oxidative stress pathway starts from CA3 sector in the hippocampus and leads to a progressive hippocampal apoptosis and atrophy (Cruz-Sánchez et al 2010). The dual effect of Hsps in execution of Aβ-induced, oxidative stress-mediated apoptosis has been demonstrated (Abdul et al 2006).…”

Section: Discussionmentioning

confidence: 99%

Collaboration of geldanamycin-activated P70S6K and Hsp70 against beta-amyloid-induced hippocampal apoptosis: an approach to long-term memory and learning

Zare

Motamedi

Digaleh

et al. 2015

Cell Stress and Chaperones

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One of the neuropathological hallmarks of Alzheimer's disease (AD) is the accumulation of betaamyloid peptides (Aβ) in senile plaques. Aβ-induced oxidative stress is believed to be responsible for degeneration and apoptosis of neurons and consequent cognitive and memory deficits. Here, we investigated the possible neuroprotective effect of the heat shock protein 90 (Hsp90) inhibitor geldanamycin (GA) against amyloid pathogenesis in adult male Wistar rats. GA or vehicle was injected into the lateral cerebral ventricles of rats 24 h before injection of Aβ (1-42) in CA1 area of hippocampus. The learning and memory of the rats were assessed 7 days after injection of Aβ using passive avoidance (PA) task. As potential contributing factors in Aβ-induced memory decline, we evaluated apoptotic markers and also used terminal-transferase UTP nick end labeling (TUNEL) technique to detect apoptosis in the hippocampus of Aβ-injected rats. Our behavioral data suggest that GA pretreatment can significantly suppress memory deficits in Aβ-injected rats. There was also not only a marked increase in Hsp70 level but also upregulated 70 kDa ribosomal protein S6 kinase (p70S6K) in the hippocampus of GA-treated groups with a reduction in apoptotic factors including caspase-3, poly (ADP-ribose) polymerase, Bax/Bcl-2 ratio, and TUNELpositive cells as well. Thus, we conclude that GA exerts its protective effects against Aβ (1-42) toxicity and memory deficits, at least in part, by upregulating of Hsp70 and P70S6K.

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“…Within the hippocampus, it is well known that the dentate gyrus-cornu ammonis (CA)3 system exhibits structural plasticity with regenerative/remodeling capacity (Popov and Bocharova, 1992;Sousa et al, 2000;McEwen, 2008). Furthermore, several studies have suggested that pyramidal cells of CA3 and granule cells of the dentate gyrus (DG) are oxidative stress-prone areas, whereas others have suggested that pyramidal cells of CA1 are more susceptible to oxidative damage (Bearden et al, 2009;Cruz-Sánchez et al, 2010;Chang et al, 2012;Huang et al, 2012Huang et al, , 2013Uysal et al, 2012). Regardless, region-specific elevation of oxidative stress within cornu ammonis areas CA1 and CA3, and DG is important and can have significant functional consequences.…”

Section: Oxidative Stress and The Brainmentioning

confidence: 99%