Search

Copyright of Brazilian Journal of Occupational Therapy / Cadernos Brasileiros de Terapia Ocupacional is the property of Cadernos de Terapia Ocupacional da UFSCar and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Brazilian Journal of Occupational Therapy / Cadernos Brasileiros de Terapia Ocupacional is the property of Cadernos de Terapia Ocupacional da UFSCar and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Background: Post Covid‐19 syndrome can cause cognitive impairment and may be associated with a higher risk of developing dementia in older people. Method: This is a cohort study that is evaluating over 12 months the functional status and cognition of elderly people after hospital discharge. One group is composed of elderly people admitted to the hospital for Covid‐19 and the other group is composed of elderly people hospitalized for other clinical reasons. The groups are evaluated with The Mattis (DRS), AD8, ADCS‐ADL, PCL‐C, GDS‐15, FIM, COPM, CFS, FSS, mMRC and SARC‐calf. We will describe the preliminary results of the first 31 patients included in the COVID‐19 group on functional status, cognition, mood and quality of life. Result: Thirty‐one patients with COVID‐19 were evaluated three months after hospital discharge. One was excluded due to previous mental disorder and another due to a request to be excluded from the study. We found a mean age of 69.55 ± 7.72 years, schooling 7.14 ± 4.48 years, 51.7% female, Charlson Comorbidity Index 2.21 ± 1.84, 48.3% with smoking history and 62.9% had incomplete vaccine protection for COVID‐19. Considering cognition, 13.9% of the sample had no impairment, 55.1% had mild cognitive impairment (MCI) (17.2% amnestic MCI and 37.9% non‐amnesic MCI) and 31% had dementia. 24.1% declared their health status and quality of life as fair or poor. Mean CFS was 4.45 ± 1.18, GDS‐15 4.28 ± 3.38, FSS 30.76 ± 19.24, PCL‐c 29.34 ± 10.41, SARC‐calf 4.03 ± 4.61. All had mMRC dyspnea classified between 1 and 4. Conclusion: There was a high prevalence of mild cognitive impairment and dementia among patients after three months of discharge, with a predominance of mild frailty due to CFS and the presence of fatigue. It is noteworthy that a quarter of the sample reported low quality of life. [ABSTRACT FROM AUTHOR]

Objective: To compare the results of neuropsychological tests, evoked potentials N200 and P300 and polymorphisms of ApoE and BDNF rs6265 between patients with normal cognition and those with mild cognitive impairment (MCI) and Alzheimer's dementia (AD).Methods: This is a cross-sectional study of elderly individuals with normal cognition and those with MCI and AD, who were submitted to evoked potential tests (N200 and P300) by means of hearing stimuli based on the auditory oddball paradigm. Genotyping was obtained by using the real-time PCR technique.Results: Sixty-five patients were evaluated as follows: 14 controls, 34 with MCI and 17 with AD. N200 latency and P300 latency and amplitude were not associated with MCI and AD diagnosis. Patients with cognitive impairment (MCI or AD) showed increase in the latencies of P300 and N200. BNDF gene was not associated with cognitive impairment.Conclusion: Latencies of N200 and P300 increased in cognitively impaired patients with the presence of ApoE ε-4 allele. [ABSTRACT FROM AUTHOR]

Objectives: In 2012, Kamboh and colleagues published a genome-wide association study that identified the DCHS2 gene (rs1466662 T/A) influencing the age at onset of Alzheimer's disease (AD). We aimed to investigate if there is association between the DCHS2 gene and amnestic mild cognitive impairment (aMCI) and AD in a sample of the Brazilian population.Methods: 143 controls, 79 aMCI and 299 AD patients were selected and submitted to the same protocol of tests. Genotyping was performed using the Real Time PCR RESULTS: Amnestic MCI patients showed a higher prevalence of AA than controls and a lower frequency of TT when compared with controls. We also stratified the sample according to the APOE ε4 status. No difference in DCHS2 genotype or allelic frequency occurred in the APOE ε4 allele carrier subgroup. Amnestic MCI patients showed a higher frequency of AA genotype and a lower frequency of TA and TT when compared with controls in APOE ε4 allele non-carrier subgroup. The allelic distribution followed the same pattern. In AD group, we observed a significant difference with a higher A allelic frequency in AD in this subgroup. A multiple logistic regression demonstrated that in APOE ε4 non-carriers, allele rs1466662 was associated to aMCI group. Different variables were associated with aMCI and AD according to APOE ε4 status in our sample. Low level of education was associated with AD, while diabetes mellitus type 2 was associated with aMCI. Copyright © 2016 John Wiley & Sons, Ltd.Conclusions: Our findings suggest a possible role for DCHS2 gene in aMCI and AD. [ABSTRACT FROM AUTHOR]

Background: Post Covid‐19 syndrome is recognized as the maintenance of disease symptoms for weeks to months after the disease has healed. It is suspected that the involvement of the ACE enzyme and IL‐6 may trigger an increased risk of dementia. Method: This is a cohort study that is evaluating over 12 months the functional status and cognition of elderly people after hospital discharge. One group is composed of elderly people admitted to the hospital for Covid‐19 and the other group is composed of elderly people hospitalized for other clinical reasons. The groups are evaluated with The Mattis (DRS), AD8, IQCODE, ADCS‐ADL, PCL‐C, GDS‐15, FIM, COPM, CFS, FSS, mMRC and SARC‐calf. We will describe the preliminary results of the first 15 patients included in the COVID‐19 group on functional status, cognition, mood and quality of life. Results: Fifteen patients with COVID‐19 were evaluated three months after hospital discharge. One was excluded due to previous mental disorder and another due to a request to be excluded from the study. We found a mean age of 67.7 ± 7.15 years, schooling 8.7 ± 4.7 years, 61.5% female, Charlson Comorbidity Index 1.9 ± 1.4, 69.2% with smoking history had incomplete vaccine protection for COVID‐19. Considering cognition, 15.4% of the sample had no impairment, 53.9% had mild cognitive impairment (MCI) (30.8% amnestic MCI and 23.1% non‐amnesic MCI) and 30.8% had dementia. 23.1% declared their health status and quality of life as fair or poor. Median CFS was 5 (3‐5), mean GDS‐15 was 4.7 ± 2.9, FSS 32.9 ± 18.9, PCL‐c 32.6 ± 12.5, SARC‐calf 3.2 ± 4.2. All had mMRC dyspnea classified between 2 and 4. Conclusion: There was a high prevalence of mild cognitive impairment and dementia among patients after three months of discharge, with a predominance of mild frailty due to CFS and the presence of fatigue. It is noteworthy that a quarter of the sample reported low quality of life. [ABSTRACT FROM AUTHOR]

Depressive symptoms are associated with cognitive-functional impairment in normal aging older adults (NA). However, less is known about this effect on people with mild Cognitive Impairment (MCI) and mild Alzheimer's disease dementia (AD). We investigated this relationship along with the NA-MCI-AD continuum by reanalyzing a previously published dataset. Participants (N=274) underwent comprehensive neuropsychological assessment including measures of Executive Function, Language/Semantic Memory, Episodic Memory, Visuospatial Abilities, Activities of Daily Living (ADL), and the Geriatric Depression Scale. MANOVA, logistic regression and chi- square tests were performed to assess the association between depression and cognitive-functional performance in each group. In the NA group, depressed participants had a lower performance compared to non-depressed participants in all cognitive and functional domains. However, the same pattern was not observed in the MCI group or in AD. The results suggest a progressive loss of association between depression and worse cognitive-functional performance along the NA-MCI-AD continuum. [ABSTRACT FROM AUTHOR]

Background:Evidences suggest that GAB2 and BDNF genes may be associated with Alzheimer's disease (AD). We aimed to investigate the GAB2 rs2373115 and BDNF rs6265 polymorphisms and the risk of AD in a Brazilian sample.Methods:269 AD patients and 114 controls were genotyped with Real-time PCR. Multifactor dimensionality reduction (MDR) was employed to explore the effects of gene–gene interactions.Results:GAB2 and BDNF were not associated with AD in our sample. Nevertheless BDNF Val allele (rs6265) presented a synergic association with the APOE ε4 allele. A multiple logistic regression demonstrated that the APOE ε4 allele and years of education were the best predictors for AD. In ε4 non-carriers sex, education and hypertension were independently correlated with AD, while in ε4 carriers we did not observe any association. The findings were further confirmed by bootstrapping method.Conclusions:Our data suggest that the interaction of BDNF and APOE has significant effect on AD. Moreover in absence of ε4, female sex, low level of education and hypertension are independently associated with AD. Interventions aimed to prevent AD should focus on these factors and also taking into account the APOE alleles. [ABSTRACT FROM AUTHOR]

Objectives The in vitro effect of a vitamin complex in generating and reducing oxidative species in peripheral blood mononuclear cells (PBMNC) and plasma of patients with Alzheimer's disease (AD) and healthy subjects (HS) was evaluated. Methods Two concentrations of a vitamin complex ([A] and [20A]) with ascorbic acid, alpha-tocopherol, and beta-carotene were incubated with either mononuclear cells or plasma. The generation of oxidizing species was measured in a luminol-dependent chemiluminescence assay and the reducing response by the MTT dye reduction assay. The levels of cytokines (interleukin [IL]-1β, IL-6, and IL-4) were measured by sandwich enzyme-linked immunosorbent assay. Results Our results demonstrated that the increase in the vitamin complex concentration reduced the reactive oxygen species (ROS) production and enhanced cellular reduction capacity in cells of AD patients in concentration [20A]. Plasma reduction capacity rose significantly for both groups (AD and HS). Concentration [A] did not alter the IL-1β production, increased IL-4 production in both groups and lowered IL-6 production in AD cells. Concentration [20A] increased pro-inflammatory cytokines (IL-1β and IL-6) and decreased IL-4 production by PBMNC of HS leading to a pro-inflammatory status. Discussion The antioxidant vitamin complex was effective in reducing oxidative stress in PBMNC of AD patients by lowering ROS production, improving cellular antioxidant capacities and modifying cytokine induced inflammation. [ABSTRACT FROM AUTHOR]

Mild cognitive impairment is a clinical condition more frequent in patients with Parkinson's disease than in general population. The nonamnestic presentations, usually characterized by executive dysfunction, are most prevalent. We present a case report of a Parkinson's disease patient diagnosed with nonamnestic mild cognitive impairment that showed complete remission of cognitive symptoms after one year. We discuss the possible causes for the remission, focusing on the treatment of medical conditions such as a major depressive episode and vitamin B12 deficiency, in addition to the change of pharmacological treatment. In a third assessment, cognitive performance remained normal. The case report highlights the importance of controlling clinical comorbidities on the assessment and followup of mild cognitive impairment, especially on Parkinson's disease. [ABSTRACT FROM AUTHOR]

Background: Individuals with mild cognitive impairment (MCI) have increased risk to convert to Alzheimer's dementia (AD). Our aim was to evaluate the role of auditory evoked potential N200 and P300 and serum level of BDNF in predicting conversion from MCI patients to AD, considering APOE and BDNF genetic background. Method: 32 MCI patients were prospectively evaluated. They underwent annual geriatric evaluation and neuropsychological assessment. Cognitive and functional status were established considering both neuropsychology and geriatrics evaluation. AD was diagnosed based on McKhann criteria. Genotyping of APOE alleles and BDNF (Val66Met) was performed by real time PCR. Participants were divided in carriers of APOE ε‐4 allele (APOE4+) and non‐carriers (APOE4‐). At baseline, BDNF concentration was assessed by ELISA methodology and, the participants were also submitted to evoked potential tests (N200 and P300) by means of auditory stimuli based on the auditory oddball paradigm. APOE+ were compared with APOE‐. Anova statistical methods, Bonferroni post‐hoc analysis, Mann Whitney and Student T tests were used, in addition to the evaluation of median, mean and standard deviation. Result: At baseline, participants had a mean age of 74.78 ± 8.35 years, 4.61 ± 3.96 years of formal education. 60.9% were female. The follow‐up mean time was 4.02 ± 1.93 years. During the follow‐up period, 11 MCI participants converted to AD (MCI‐c) and 22 remained stable (MCI‐nc). 34.9% of total sample were APOE+. We did not observe any statistical difference in N200 latency (p = 0.715), P300 latency (p = 0.993) and P300 amplitude (p = 0.574) between MCI‐c and MCI‐nc. However, among APOE+ MCI patients who converted to AD, a significant difference was observed in P300 latency in relation to MCI‐nc (419.63 ± 29.74 versus 349.85 ± 35.82ms, p value: 0.023). We did not observe a relationship between BDNF serum level and conversion to AD (p: 0.061). Nevertheless, in Val/Val BDNF genotype, higher BDNF was associated with conversion to AD (10093.03 ± 3055.49pg / ml versus 5755, 85 ± 1873.20pg / ml, p‐value: 0.017). Conclusion: P300 latency and serum BDNF level in APOE+ and Val/Val BDNF genotype patients are related to conversion of MCI to AD. [ABSTRACT FROM AUTHOR]

Background: Psychiatric disorders are among etiologies for Mild Cognitive Impairment (MCI), one of the main one is depression. The relationship between depression and Alzheimer's disease (AD) is not yet fully understood and it is considered both, isolated risk factor and prodrome stage of AD. The aim of this work is to investigate if older adults with MCI associated with significant depressive symptoms, compared with those without these symptoms, will have different executive functions outcomes after one‐year follow‐up. Method: Repeated measures ANCOVA with Bonferroni post‐hoc analysis was used with cognitive variables at baseline and follow up evaluation as dependent, presence of significative depression symptoms at baseline as independent while controlling for covariates age, gender and years of formal education. Depressive symptoms were measured by 15‐item geriatric depression scale and the cutoff point was 6. Executive functions as inhibitory control e cognitive flexibility were assessed by Five Digit Test, working memory by Digit Span Test and phonemic verbal fluency by letter S. Patients started depression treatment at baseline. Result: Were included 170 participants (125 without depressive symptoms and 45 with symptoms), mean age 74.44, 68 women, mean years of formal education was 4,54. Among these, 99 (29 with depressive symptoms) complete all tests in the two assessments. Due to cognitive impairment, some of them were unable to even start cognitive flexibility test. Results indicated there was a significant effect of depression symptoms at baseline on cognitive flexibility ability [F (1.94) = 7,271, p = 0.008). Participants with depression presented a significant improvement (p = 0.006) on cognitive flexibility average from baseline (11.60) to the end of follow up (7.24). For those without symptoms of depression at baseline, the averages were 6.32 at baseline and 5.98 at follow‐up. There was no significant effect of depressive symptoms on the other cognitive skills assessed when considering these covariates. Conclusion: Comparing participants with and without depression symptoms at baseline, there was an improvement in cognitive flexibility in the former group. We think this result could be related to effect of depression treatment. [ABSTRACT FROM AUTHOR]

Background: Depression and diabetes mellitus (DM) are associated with an increased risk for dementia and mild cognitive impairment (MCI). Subcortical anatomical changes associated with processing speed impairment are shared by both DM subtypes. This profile is similar for depression, a condition in which processing speed and executive functions mediate deficits in other domains. Thus, the aim of this work is to investigate the interaction between diabetes and depression with executive functions and processing speed on older adults with mild cognitive impairment. Method: 76 elderly people aged 60 to 96 years (M=75, SD=7.5) from UFMG outpatient clinic for older adults on Instituto Jenny de Andrade Faria participated in the study, predominantly low formal education (M=4, SD=4.5), 23 with significative depressive symptoms, 21 with diabetes mellitus, and 7 with both conditions. Multivariate analysis of variance was used (with cognitive variables as dependent, depression and diabetes as factors and age and education as covariates). Statistical method used was GLM and post‐hoc LSD analysis (Fisher's least significant difference). The level of significance adopted was 0.05. Processing speed, inhibitory control and cognitive flexibility were the study dependent variables, measured by the Five Digit Test. Result: Diabetes is associated with processing speed impairment (F =5,505; p =0,022; partial η2 = 0,073) and depression symptoms with decrease in inhibitory control (F =6,467; p =0,013; partial η2 = 0,085). The interaction between two conditions is associated with poorer performance in inhibitory control (F =6,423; p =0,014; partial η2 = 0,084). Conclusion: Subcortical anatomical changes associated with processing speed impairment are shared by depression and diabetes mellitus. But when two conditions are compared on a similar group of older adults with mild cognitive impairment, executive functions decline is more expressive than processing speed on patients with depression. These results corroborate those found in the literature, where the cognitive decline in patients with depression is mediated by executive functions and on diabetes by processing speed. [ABSTRACT FROM AUTHOR]

Background: Although randomized controlled trials have not confirmed cognitive impairing effects of statins, continuing evidence suggests statins have the ability to cause reversible cognitive impairment in some patients. Paradoxically, statins have also been shown to decrease risk of dementia, Alzheimer's disease, and to improve cognitive impairment in some cases. However, randomized controlled trials have similarly failed to find the beneficial effect. We conducted evaluate the effect of statin on the conversion of mild cognitive impairment (MCI) to dementia in a Cohort of elderly individuals without functional and cognitive impaiment (NC) and with MCI patients. Method: Cohort was reassessed annually by geriatricians and neuropsychologists for an average period of 3.01 ± 1.43 years. The effect of statin on cognition was evaluated when it was in use throughout the follow‐up period and, it was in use at any time during the follow‐up. Chi‐square and Fisher tests (categorical variables) and student t tests, ANOVA, Mann Whiney (continuous variables) were used. Results: 176 individuals were selected (53 CG, 111 with amnestic MCI ‐ aMCI‐ and 12 with non‐amnestic MCI ‐naMCI), aged 76.52 ± 7.27 years, 69% female and 3.61 ± 3.23 years of schooling. We observed conversion of aMCI to dementia in 27 participants (92.6% Alzheimer dementia), corresponding to a conversion rate of 24.3%. In the aMCI group, the remission rate was 13.5%. 51.1% of the sample received statin at some point during the follow‐up and 30.7% used it throughout the study. 98.8% of prescribed statins had moderate potency. Comparing stable MCI group throughout the study with the group which progressed to dementia, the group that used it any time during the follow‐up analysis showed a p‐value of 0.104, whereas the group that used it during the entire follow‐up showed a p‐value of 0.166. Comparing remission and conversion groups, the one that used statin any time during the follow‐up showed a p‐value of 0.542, patients who received statin during the entire follow‐up had a p‐value of 0.746. Conclusion: Statins were not associated with conversion from aMCI to dementia, even when used throughout the entire follow‐up. [ABSTRACT FROM AUTHOR]