scholarly journals Systemic Oxidative Stress and Conversion to Dementia of Elderly Patients with Mild Cognitive Impairment

2014 ◽  
Vol 2014 ◽  
pp. 1-7 ◽  
Author(s):  
Carlo Cervellati ◽  
Arianna Romani ◽  
Davide Seripa ◽  
Eleonora Cremonini ◽  
Cristina Bosi ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cognitive Impairment ◽  
Mild Cognitive Impairment ◽  
Late Onset ◽  
Healthy Controls ◽  
Prodromal Phase ◽  
Systemic Oxidative Stress ◽  
By Products

Mild cognitive impairment (MCI) is regarded as a prodromal phase of late onset Alzheimer’s disease (LOAD). It has been proposed that oxidative stress (OxS) might be implicated in the pathogenesis of LOAD. The aim of this study was to investigate whether a redox imbalance measured as serum level of hydroperoxides (i.e., by-products of lipid peroxidation) and/or serum antioxidant capacity might be predictive of the clinical progression of MCI to LOAD. The levels of these two markers were measured in 111 patients with MCI (follow-up:2.0 ± 0.6years), 105 patients with LOAD, and 118 nondemented healthy controls. Multivariate analysis adjusted for potential confounding factors, including age, gender, smoking, and comorbidities, showed a significant increase (P<0.05) in baseline levels of OxS in MCI and LOAD as compared to cognitive healthy controls. No differences in either of OxS markers were found by comparing MCI patients who converted (n = 29) or not converted (n = 82) to LOAD. Overall, these results suggest that systemic OxS might be a precocious feature of MCI and LOAD. However, the role of OxS as an early prognostic marker of progression to LOAD needs further investigations.

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

2013 ◽  
Vol 10 (4) ◽  
pp. 365-372 ◽  
Author(s):  
Carlo Cervellati ◽  
Eleonora Cremonini ◽  
Cristina Bosi ◽  
Stefania Magon ◽  
Amedeo Zurlo ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cognitive Impairment ◽  
Mild Cognitive Impairment ◽  
Older Patients ◽  
Late Onset ◽  
Systemic Oxidative Stress

scholarly journals Oxidative stress and antioxidant defenses in mild cognitive impairment: a systematic review and meta-analysis.

2021 ◽  
Author(s):  
gallayaporn nantachai ◽  
Asara Vasupanrajit ◽  
Chavit Tunvirachaisakul ◽  
Marco Solmi ◽  
Michael Maes
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Cognitive Impairment ◽  
Mild Cognitive Impairment ◽  
Web Of Science ◽  
Reduced Glutathione ◽  
Meta Analysis ◽  
Antioxidant Defenses ◽  
Healthy Controls ◽  
Standardized Mean Difference

This study aims to systematically review and meta-analyze the nitro-oxidative stress (O&NS)/antioxidant (ANTIOX) ratio in the peripheral blood of people with mild cognitive impairment (MCI). We searched PubMed, Scopus, Google Scholar, and Web of Science for articles published from inception until July 31, 2021. Forty-six studies on 3.798 MCI individuals and 6.063 healthy controls were included. The O&NS/ANTIOX ratio was significantly higher in MCI than in controls with a Standardized Mean Difference (SMD)=0.378 (95% CI: 0.250; 0.506). MCI individuals showed increased lipid peroxidation (SMD=0.774, 95%CI: 4.416; 1.132) and O&NS-associated toxicity (SMD=0.621, CI: 0.377; 0.865) and reduced glutathione (GSH) defenses (SMD=0.725, 95%CI: 0.269; 1.182) as compared with controls. MCI was also accompanied by significantly increased homocysteine (SMD=0.320, CI: 0.059; 0.581), but not protein oxidation, and lowered non-vitamin (SMD=0.347, CI: 0.168; 0.527) and vitamin (SMD=0.564, CI: 0.129; 0.999) antioxidant defenses. The results show that MCI is at least in part due to increased neuro-oxidative toxicity and suggest that treatments targeting lipid peroxidation and the GSH system may be used to treat or prevent MCI.

scholarly journals Oxidative Stress and Antioxidant Defenses in Mild Cognitive Impairment: A Systematic Review and Meta-Analysis

2021 ◽  
Author(s):  
Gallayaporn Nantachai ◽  
Asara Vasupanrajit ◽  
Chavit Tunvirachaisakul ◽  
Marco Solmi ◽  
Michael Maes Michael Maes
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Cognitive Impairment ◽  
Mild Cognitive Impairment ◽  
Web Of Science ◽  
Reduced Glutathione ◽  
Meta Analysis ◽  
Antioxidant Defenses ◽  
Healthy Controls ◽  
Standardized Mean Difference

This study aims to systematically review and meta-analyze the nitro-oxidative stress (O&amp;NS)/antioxidant (ANTIOX) ratio in the peripheral blood of people with mild cognitive impairment (MCI). We searched PubMed, Scopus, Google Scholar, and Web of Science for articles published from inception until July 31, 2021. Forty-six studies on 3.798 MCI individuals and 6.063 healthy controls were included. The O&amp;NS/ANTIOX ratio was significantly higher in MCI than in controls with a Standardized Mean Difference (SMD)=0.378 (95% CI: 0.250; 0.506). MCI individuals showed increased lipid peroxidation (SMD=0.774, 95%CI: 4.416; 1.132) and O&amp;NS-associated toxicity (SMD=0.621, CI: 0.377; 0.865) and reduced glutathione (GSH) defenses (SMD=0.725, 95%CI: 0.269; 1.182) as compared with controls. MCI was also accompanied by significantly increased homocysteine (SMD=0.320, CI: 0.059; 0.581), but not protein oxidation, and lowered non-vitamin (SMD=0.347, CI: 0.168; 0.527) and vitamin (SMD=0.564, CI: 0.129; 0.999) antioxidant defenses. The results show that MCI is at least in part due to increased neuro-oxidative toxicity and suggest that treatments targeting lipid peroxidation and the GSH system may be used to treat or prevent MCI.

The dual role of cognitive reserve in subjective cognitive decline and mild cognitive impairment: a 7-year follow-up study

2019 ◽  
Vol 266 (2) ◽  
pp. 487-497 ◽  
Author(s):  
Salvatore Mazzeo ◽  
Sonia Padiglioni ◽  
Silvia Bagnoli ◽  
Laura Bracco ◽  
Benedetta Nacmias ◽  
...  
Keyword(s):  
Cognitive Impairment ◽  
Mild Cognitive Impairment ◽  
Cognitive Decline ◽  
Cognitive Reserve ◽  
Dual Role ◽  
Subjective Cognitive Decline ◽  
Follow Up Study

PON-1 and ferroxidase activities in older patients with mild cognitive impairment, late onset Alzheimer’s disease or vascular dementia

2015 ◽  
Vol 53 (7) ◽  
Author(s):  
Carlo Cervellati ◽  
Arianna Romani ◽  
Carlo M. Bergamini ◽  
Cristina Bosi ◽  
Juana Maria Sanz ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cognitive Impairment ◽  
Mild Cognitive Impairment ◽  
Vascular Dementia ◽  
Late Onset ◽  
Large Body ◽  
Multivariate Logistic Regression Analysis ◽  
Paraoxonase 1 ◽  
Prodromal Phase

AbstractA large body of evidence suggests that not only cerebral but also systemic oxidative stress (OxS) might be involved in the pathogenesis of late onset Alzheimer’s disease (LOAD) and vascular dementia (VAD), as well as of the prodromal phase of dementia, the so-called mild cognitive impairment (MCI). In the present study, we evaluated whether paraoxonase 1 (PON-1) and ferroxidase (FeOx) activities, because of their well acknowledged effectiveness as systemic antioxidants, might be associated with dementia and/or MCI.Serum arylesterase and paraoxonase of PON-1, along with FeOx I (ceruloplasmin-related) and II activities were assessed in 223 MCI, 162 LOAD, 65 VAD patients, and in 143 older normal cognitive controls.Among the enzymatic activities examined, only arylesterase significantly changed across the groups (ANOVA: p<0.001), with similar lower levels in MCI, LOAD, and VAD compared to controls. By multivariate logistic regression analysis we showed that, in respect to controls, low levels (under the median value) of serum arylesterase were independently associated with an increase in the likelihood of being affected by LOAD [odds ratio (OR) 2.8, 95% confidence interval (CI) 1.5–5.0], VAD (OR 2.7, 95% CI 1.2–6.2), or MCI (OR 2.3, 95% CI 1.3–3.8).Overall, our results suggest that depression of PON-1, and in particular, of arylesterase activity, in serum might be an early feature of dementia-related diseases. Further longitudinal exploration of the role of this enzyme in the onset and progression of these disorders are required.

The Impact of Depression on the Development of Mild Cognitive Impairment over 3 Years of Follow-Up: A Population-Based Study

2017 ◽  
Vol 43 (3-4) ◽  
pp. 155-169 ◽  
Author(s):  
Elvira Lara ◽  
Ai Koyanagi ◽  
Joan Domènech-Abella ◽  
Marta Miret ◽  
Jose Luis Ayuso-Mateos ◽  
...  
Keyword(s):  
Cognitive Impairment ◽  
Mild Cognitive Impairment ◽  
Multinomial Logistic Regression ◽  
Population Sample ◽  
Composite International Diagnostic Interview ◽  
Incidence Rates ◽  
Prodromal Phase ◽  
Objective Evidence ◽  
The Impact

Background/Aims: In the absence of effective treatments for dementia, major efforts are being directed towards identifying the risk factors of the prodromal phase of the disease. We report the incidence rates of mild cognitive impairment (MCI) in a Spanish population sample and assess the effect of depression at baseline on incident MCI (or MCI subtypes) at a 3-year follow-up. Methods: A total of 1,642 participants (age ≥50 years) were examined as part of a Spanish nationally representative longitudinal study. MCI was defined as the presence of cognitive concerns, objective evidence of impairment in one or more cognitive domains, preservation of independence in functional abilities, and no dementia. Depression was assessed through an adaptation of the Composite International Diagnostic Interview (CIDI 3.0). Binary and multinomial logistic regression analyses were carried out to assess the associations. Results: The overall MCI incidence rate was 33.19 (95% CI = 26.02, 43.04) per 1,000 person-years. Depression at baseline predicted the onset of MCI at follow-up after controlling for sociodemographics, cognitive functioning, and other physical health conditions (OR = 2.79; 95% CI = 1.70, 4.59). The effect of baseline depression on incident MCI subtypes was as follows: amnestic MCI, OR = 3.81 (95% CI = 1.96, 7.43); nonamnestic MCI, OR = 2.03 (95% CI = 0.98, 4.21). Conclusion: Depression significantly increases the risk for MCI. Targeting depression among those at risk for dementia may help delay or even prevent the onset of dementia.

Elucidating the risk factors for progression from amyloid-negative amnestic mild cognitive impairment to dementia

2020 ◽  
Vol 17 ◽  
Author(s):  
Hyung-Ji Kim ◽  
Jae-Hong Lee ◽  
E-nae Cheong ◽  
Sung-Eun Chung ◽  
Sungyang Jo ◽  
...  
Keyword(s):  
Risk Factors ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cognitive Impairment ◽  
Mild Cognitive Impairment ◽  
Amnestic Mild Cognitive Impairment ◽  
Amyloid Pet ◽  
Clinical Progression ◽  
Amnestic Mci

Background: Amyloid PET allows for the assessment of amyloid β status in the brain, distinguishing true Alzheimer’s disease from Alzheimer’s disease-mimicking conditions. Around 15–20% of patients with clinically probable Alzheimer’s disease have been found to have no significant Alzheimer’s pathology on amyloid PET. However, a limited number of studies had been conducted this subpopulation in terms of clinical progression. Objective: We investigated the risk factors that could affect the progression to dementia in patients with amyloid-negative amnestic mild cognitive impairment (MCI). Methods: This study was a single-institutional, retrospective cohort study of patients over the age of 50 with amyloidnegative amnestic MCI who visited the memory clinic of Asan Medical Center with a follow-up period of more than 36 months. All participants underwent brain magnetic resonance imaging (MRI), detailed neuropsychological testing, and fluorine-18[F18]-florbetaben amyloid PET. Results: During the follow-up period, 39 of 107 patients progressed to dementia from amnestic MCI. In comparison with the stationary group, the progressed group had a more severe impairment in verbal and visual episodic memory function and hippocampal atrophy, which showed an Alzheimer’s disease-like pattern despite the lack of evidence for significant Alzheimer’s disease pathology. Voxel-based morphometric MRI analysis revealed that the progressed group had a reduced gray matter volume in the bilateral cerebellar cortices, right temporal cortex, and bilateral insular cortices. Conclusion: Considering the lack of evidence of amyloid pathology, clinical progression of these subpopulation may be caused by other neuropathologies such as TDP-43, abnormal tau or alpha synuclein that lead to neurodegeneration independent of amyloid-driven pathway. Further prospective studies incorporating biomarkers of Alzheimer’s diseasemimicking dementia are warranted.

Cerebrovascular and Neurodegenerative Pathologies in Long-Term Stable Mild Cognitive Impairment

2021 ◽  
pp. 1-15
Author(s):  
Manu J. Sharma ◽  
Brandy L. Callahan
Keyword(s):  
Cognitive Impairment ◽  
Mild Cognitive Impairment ◽  
Cerebral Amyloid Angiopathy ◽  
Neurofibrillary Tangles ◽  
Small Vessel Disease ◽  
Significant Proportion ◽  
Amyloid Angiopathy ◽  
Prodromal Phase ◽  
Cerebral Amyloid

Background: Mild cognitive impairment (MCI) is considered by some to be a prodromal phase of a progressive disease (i.e., neurodegeneration) resulting in dementia; however, a substantial portion of individuals (ranging from 5–30%) remain cognitively stable over the long term (sMCI). The etiology of sMCI is unclear but may be linked to cerebrovascular disease (CVD), as evidence from longitudinal studies suggest a significant proportion of individuals with vasculopathy remain stable over time. Objective: To quantify the presence of neurodegenerative and vascular pathologies in individuals with long-term (>5-year) sMCI, in a preliminary test of the hypothesis that CVD may be a contributor to non-degenerative cognitive impairment. We expect frequent vasculopathy at autopsy in sMCI relative to neurodegenerative disease, and relative to individuals who convert to dementia. Methods: In this retrospective study, using data from the National Alzheimer’s Coordinating Center, individuals with sMCI (n = 28) were compared to those with MCI who declined over a 5 to 9-year period (dMCI; n = 139) on measures of neurodegenerative pathology (i.e., Aβ plaques, neurofibrillary tangles, TDP-43, and cerebral amyloid angiopathy) and CVD (infarcts, lacunes, microinfarcts, hemorrhages, and microbleeds). Results: Alzheimer’s disease pathology (Aβ plaques, neurofibrillary tangles, and cerebral amyloid angiopathy) was significantly higher in the dMCI group than the sMCI group. Microinfarcts were the only vasculopathy associated with group membership; these were more frequent in sMCI. Conclusion: The most frequent neuropathology in this sample of long-term sMCI was microinfarcts, tentatively suggesting that silent small vessel disease may characterize non-worsening cognitive impairment.

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