Systemic Oxidative Stress in Older Patients with Mild Cognitive Impairment or Late Onset Alzheimer&amp;apos;s Disease

Cervellati, Carlo; Cremonini, Eleonora; Bosi, Cristina; Magon, Stefania; Zurlo, Amedeo; Bergamini, Carlo M.; Zuliani, Giovanni

doi:10.2174/1567205011310040003

Cited by 74 publications

(72 citation statements)

References 44 publications

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“…Even at the stage of MCI, damage inflicted by oxidative stress to key proteins leads to deficiencies in systems important to the brain, such as neurotransmitter release, cell signaling, energy metabolism, and the proteasome, which might lead to the progression and pathogenesis of cognitive decline (7). In addition, oxidative parameters in the circulation were also higher in patients from MCI groups than in the control group (23,24). In line with these findings, the levels of nitrotyrosine and 8-iso-PGF2a in this study showed a similar trend and were higher in elderly patients with type 2 diabetes with MCI than in those without MCI.…”

Section: Discussionmentioning

confidence: 99%

Association of Plasma DPP4 Activity With Mild Cognitive Impairment in Elderly Patients With Type 2 Diabetes: Results From the GDMD Study in China

et al. 2016

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OBJECTIVEHyperglycemia, inflammation, and oxidative stress are thought to be involved in the pathogenesis of cognitive decline. Dipeptidyl peptidase-4 (DPP4) is a newly identified adipokine related to these risk factors. Hence, we aimed to investigate the association between plasma DPP4 activities and mild cognitive impairment (MCI) in elderly patients with type 2 diabetes. RESEARCH DESIGN AND METHODSWe evaluated plasma DPP4 activity, inflammatory markers, and oxidative stress parameters in a cross-sectional sample of 1,160 patients with type 2 diabetes aged 60 years or older in China. MCI was diagnosed based on criteria established by the National Institute on Aging-Alzheimer's Association workgroups RESULTSPatients in the highest quartile of DPP4 activity had higher HbA 1c , interleukin 6 (IL-6), CRP, nitrotyrosine, 8-iso-PGF2a, and lower Montreal Cognitive Assessment (MoCA) scores compared with subjects in the lowest quartile (P < 0.001). In the highest DPP4 quartile, MCI risk was higher (odds ratio 3.49; 95% CI 1.97-4.57) than in the lowest quartile after adjustment for potential confounders. The risk for MCI increased more with higher levels of DPP4 activity, IL-6, CRP, nitrotyrosine, and 8-iso-PGF2a (P < 0.05), but not with higher levels of HbA 1c . CONCLUSIONSThis study shows that increased DPP4 activities are independently associated with MCI in elderly patients with type 2 diabetes. The mechanisms might be partly explained by the effect of DPP4 on inflammation and oxidative stress. These observations raise further interest in DPP4 activity for its potential effect on these MCI-related risk factors as a biological marker or even a possible therapeutic target for MCI.Type 2 diabetes is associated with an increased risk of accelerated age-related cognitive impairment and a higher incidence of dementia (1). Dementia is generally preceded by an intermediate stage, termed mild cognitive impairment (MCI), in which patients have cognitive complaints and objective disturbances on cognitive tests but in which their daily functioning is largely preserved (2). Although not all

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Section: Discussionmentioning

confidence: 99%

Association of Plasma DPP4 Activity With Mild Cognitive Impairment in Elderly Patients With Type 2 Diabetes: Results From the GDMD Study in China

et al. 2016

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“…There is growing evidence to support an association between oxidative stress and neurodegenerative diseases [52], mild neurocognitive disorder [53], and neuropsychological disorders including depression/anxiety [54]. For example, Fig.…”

Section: Resolution Of Inflammation: Capitalizing On Nature's Defensementioning

confidence: 99%

N-Palmitoylethanolamine and Neuroinflammation: a Novel Therapeutic Strategy of Resolution

et al. 2015

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Inflammation is fundamentally a protective cellular response aimed at removing injurious stimuli and initiating the healing process. However, when prolonged, it can override the bounds of physiological control and becomes destructive. Inflammation is a key element in the pathobiology of chronic pain, neurodegenerative diseases, stroke, spinal cord injury, and neuropsychiatric disorders. Glia, key players in such nervous system disorders, are not only capable of expressing a pro-inflammatory phenotype but respond also to inflammatory signals released from cells of immune origin such as mast cells. Chronic inflammatory processes may be counteracted by a program of resolution that includes the production of lipid mediators endowed with the capacity to switch off inflammation. These naturally occurring lipid signaling molecules include the N-acylethanolamines, N-arachidonoylethanolamine (an endocannabinoid), and its congener N-palmitoylethanolamine (palmitoylethanolamide or PEA). PEA may play a role in maintaining cellular homeostasis when faced with external stressors provoking, for example, inflammation. PEA is efficacious in mast cell-mediated models of neurogenic inflammation and neuropathic pain and is neuroprotective in models of stroke, spinal cord injury, traumatic brain injury, and Parkinson disease. PEA in micronized/ultramicronized form shows superior oral efficacy in inflammatory pain models when compared to naïve PEA. Intriguingly, while PEA has no antioxidant effects per se, its co-ultramicronization with the flavonoid luteolin is more efficacious than either molecule alone. Inhibiting or modulating the enzymatic breakdown of PEA represents a complementary therapeutic approach to treat neuroinflammation. This review is intended to discuss the role of mast cells and glia in neuroinflammation and strategies to modulate their activation based on leveraging natural mechanisms with the capacity for self-defense against inflammation.

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“…Of the remaining 35 studies, 6 studies were excluded for irrelevant outcomes and 5 studies were excluded for no usable data. Thus, 24 studies were finally included into the meta-analysis [14][15][16][17][18][19][20][21][22][23][24][28][29][30][31][32][33][34][35][36][37][38][39][40]. Among those 24 studies, 21 were case-control studies comparing serum uric acid levels in Alzheimer's disease patients with healthy controls [14-24, 28-32, 36-40] and 3 studies were cohort studies assessing risk of Alzheimer's disease in individuals with various categories of serum uric acid levels [33][34][35].…”

Section: Characteristics Of Included Studiesmentioning

confidence: 99%

“…Among those 24 studies, 21 were case-control studies comparing serum uric acid levels in Alzheimer's disease patients with healthy controls [14-24, 28-32, 36-40] and 3 studies were cohort studies assessing risk of Alzheimer's disease in individuals with various categories of serum uric acid levels [33][34][35]. Among those 24 studies, 19 studies were published in English [14][15][16][17][18][19][20][21][22][23][24][28][29][30][31][32][33][34][35] while the other 5 studies were published in Chinese [36][37][38][39][40]. Those 21 case-control studies included a total of 1128 cases of Alzheimer's disease and 2498 controls without Alzheimer's disease [14-24, 28-32, 36-40].…”

Section: Characteristics Of Included Studiesmentioning

confidence: 99%

Inverse Association Between Serum Uric Acid Levels and Alzheimer’s Disease Risk

Hou

et al. 2015

Mol Neurobiol

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The association between Alzheimer's disease and uric acid levels had gained great interest in recent years, but there was still lack of definite evidence. A systematic review and meta-analysis of relevant studies was performed to comprehensively estimate the association. Relevant studies published before October 26, 2014, were searched in PubMed, Embase, and China Biology Medicine (CBM) databases. Study-specific data were combined using random-effects or fixed-effects models of meta-analysis according to between-study heterogeneity. Twenty-four studies (21 case-control and 3 cohort studies) were finally included into the meta-analysis. Those 21 case-control studies included a total of 1128 cases of Alzheimer's disease and 2498 controls without Alzheimer's disease. Those 3 cohort studies included a total of 7327 participants. Meta-analysis showed that patients with Alzheimer's disease had lower levels of uric acid than healthy controls (weighted mean difference (WMD) = -0.77 mg/dl, 95% CI -2.28 to -0.36, P = 0.0002). High serum uric acid levels were significantly associated with decreased risk of Alzheimer's disease (risk ratio (RR) = 0.66, 95% CI 0.52-0.85, P = 0.001). There was low risk of publication bias in the meta-analysis. There is an inverse association between serum uric acid levels and Alzheimer's disease. High serum uric acid level is a protective factor of Alzheimer's disease.

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Systemic Oxidative Stress in Older Patients with Mild Cognitive Impairment or Late Onset Alzheimer's Disease

Cited by 74 publications

References 44 publications

Association of Plasma DPP4 Activity With Mild Cognitive Impairment in Elderly Patients With Type 2 Diabetes: Results From the GDMD Study in China

Association of Plasma DPP4 Activity With Mild Cognitive Impairment in Elderly Patients With Type 2 Diabetes: Results From the GDMD Study in China

N-Palmitoylethanolamine and Neuroinflammation: a Novel Therapeutic Strategy of Resolution

Inverse Association Between Serum Uric Acid Levels and Alzheimer’s Disease Risk

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