scholarly journals Saccular Impairment in Alzheimer’s Disease Is Associated with Driving Difficulty

2017 ◽  
Vol 44 (5-6) ◽  
pp. 294-302 ◽  
Author(s):  
Eric X. Wei ◽  
Esther S. Oh ◽  
Aisha Harun ◽  
Matthew Ehrenburg ◽  
Yuri Agrawal
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cognitive Function ◽  
Spatial Cognition ◽  
Fear Of Falling ◽  
Regression Analyses ◽  
Memory Clinic ◽  
Vestibular Loss ◽  
Road Map ◽  
The Impact

Background/Aims: Patients with Alzheimer’s disease (AD) experience increased rates of vestibular loss. Recent studies suggest that saccular impairment in mild cognitive impairment (MCI) and AD patients is associated with impaired spatial cognitive function. However, the impact of saccular impairment on everyday behaviors that rely on spatial cognitive function is unknown. Methods: We recruited 60 patients (21 MCI and 39 AD) from an interdisciplinary Memory Clinic. Saccular function was measured, and a visuospatial questionnaire was administered to assess whether participants experienced impairments in terms of driving difficulty, losing objects, falls, and fear of falling. Results: In multiple logistic regression analyses, MCI and AD patients with bilateral saccular impairment had a significant, greater than 12-fold odds of driving difficulty (OR 12.1, 95% CI 1.2, 117.7) compared to MCI and AD patients with normal saccular function, and the association appears to be mediated by spatial cognition as measured by the Money Road Map Test. Conclusion: This study suggests a novel link between saccular impairment and driving difficulty in MCI and AD patients and demonstrates that driving difficulty may be a real-world manifestation of impaired spatial cognition associated with saccular impairment.

Modelling the impact of functionality, cognition, and mood state on awareness in people with Alzheimer’s disease

2019 ◽  
pp. 1-11
Author(s):  
Anna Fischer ◽  
Marcia Cristina Nascimento Dourado ◽  
Jerson Laks ◽  
Jesus Landeira-Fernandez ◽  
Robin G. Morris ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cognitive Function ◽  
Mood State ◽  
Depressive Mood ◽  
Medium Effect ◽  
Underlying Structure ◽  
Competing Models ◽  
The Impact ◽  
The Relationship

AbstractObjectives:To investigate the nature of the relationship between cognitive function, mood state, and functionality in predicting awareness in a non-clinically depressed sample of participants with mild to moderate Alzheimer’s disease (AD) in Brazil.Methods:People with AD (PwAD) aged 60 years or older were recruited from an outpatient unit at the Center of AD of the Federal University of Rio de Janeiro, Brazil. Measures of awareness of condition (Assessment Scale of the Psychosocial Impact of the Diagnosis of Dementia), cognitive function (Mini-Mental State Examination), mood state (Cornell Scale for Depression in Dementia), and functionality (Pfeffer Functional Activities Questionnaire) were applied to 264 people with mild to moderate AD and their caregivers. Hypotheses were tested statistically using SEM approach. Three competing models were compared.Results:The first model, in which the influence of mood state and cognitive function on awareness was mediated by functionality, showed a very good fit to the data and a medium effect size. The competing models, in which the mediating variables were mood state and cognitive function, respectively, only showed poor model fit.Conclusion:Our model supports the notion that the relationship between different factors and awareness in AD is mediated by functionality and not by depressive mood state or cognitive level. The proposed direct and indirect effects on awareness are discussed, as well as the missing direct influence of mood state on awareness. The understanding of awareness in dementia is crucial and our model gives one possible explanation of its underlying structure in AD.

scholarly journals Anxiety Impacts Consent Capacity to Treatment in Alzheimer's Disease

2021 ◽  
Vol 12 ◽  
Author(s):  
Yuka Kato ◽  
Teruyuki Matsuoka ◽  
Yoko Eguchi ◽  
Kiyoko Iiboshi ◽  
Hiroyuki Koumi ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cognitive Function ◽  
Linear Regression ◽  
Assessment Tool ◽  
Psychiatric Symptoms ◽  
Regression Equations ◽  
Regression Analyses ◽  
Alternative Treatments ◽  
Capacity For Consent

This study aimed to clarify how behavioral and psychological symptoms of dementia (BPSD) and cognitive function affect the decision-making capacity of persons with Alzheimer's disease (AD) in a real informed consent situation about anti-dementia drug prescriptions. The participants were 76 patients with AD. We used the MacArthur Competence Assessment Tool to assess the capacity for consent to treatment (MacCAT-T). We simultaneously used the Mini-Mental State Examination, Executive Interview, Executive Clock Drawing Task, Logical Memory I of the Wechsler Memory Scale-Revised (LM I), LM II, and Neuropsychiatric Inventory (NPI) to assess cognitive function and psychiatric symptoms. We calculated the correlations between the MacCAT-T scores and the demographic, neuropsychological, and psychiatric variables. Once the univariable correlations were determined, we performed simple linear regression analyses to examine if the regression equations were significant. In the final analyses, we incorporated significant variables into stepwise multiple linear regression analyses to determine the most significant predictors of mental capacity. Age (β = −0.34), anxiety (β = −0.27), and LM I (β = 0.26) were significant predictors of “understanding” (adjusted R2 = 0.29). LM II (β = 0.39), anxiety (β = −0.29), and education (β = 0.21) were significant predictors of “understanding of alternative treatments” (adjusted R2 = 0.30). Anxiety (β = −0.36) and age (β = −0.22) were significant predictors of “appreciation” (adjusted R2 = 0.18). Age (β = −0.31) and anxiety (β = −0.28) were significant predictors of explained variance in “reasoning” (adjusted R2 = 0.17). Patients with anxiety had lower scores on all five MacCAT-T subscales: “understanding,” without 3.8 [SD = 1.2] vs. with 2.6 [SD = 1.1]; “understanding of alternative treatments,” without 2.9 [SD = 2.2] vs. with 1.3 [SD = 1.8]; “appreciation,” without 2.9 [SD = 1.1] vs. with 1.9 [SD = 1.2]; “reasoning,” without 4.0 [SD = 2.0] vs. with 2.7 [SD = 1.7]; and “expressing a choice,” without 1.9 [SD = 0.4] vs. with 1.5 [SD = 0.6]. Considering the effects of BPSD, cognitive function, and age/education when assessing consent capacity in persons with AD is important. Reducing anxiety may contribute to improved capacity in persons with AD.

scholarly journals Differential effects of risk factors on the cognitive trajectory of early- and late-onset Alzheimer’s disease

2021 ◽  
Vol 13 (1) ◽  
Author(s):  
Jaeho Kim ◽  
Sook-Young Woo ◽  
Seonwoo Kim ◽  
Hyemin Jang ◽  
Junpyo Kim ◽  
...  
Keyword(s):  
Risk Factors ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cognitive Function ◽  
Cognitive Decline ◽  
Late Onset ◽  
Low Education ◽  
Rapid Cognitive Decline ◽  
Function Language ◽  
The Impact

Abstract Background Although few studies have shown that risk factors for Alzheimer’s disease (AD) are associated with cognitive decline in AD, not much is known whether the impact of risk factors differs between early-onset AD (EOAD, symptom onset < 65 years of age) versus late-onset AD (LOAD). Therefore, we evaluated whether the impact of Alzheimer’s disease (AD) risk factors on cognitive trajectories differ in EOAD and LOAD. Methods We followed-up 193 EOAD and 476 LOAD patients without known autosomal dominant AD mutation for 32.3 ± 23.2 months. Mixed-effects model analyses were performed to evaluate the effects of APOE ε4, low education, hypertension, diabetes, dyslipidemia, and obesity on cognitive trajectories. Results APOE ε4 carriers showed slower cognitive decline in general cognitive function, language, and memory domains than APOE ε4 carriers in EOAD but not in LOAD. Although patients with low education showed slower cognitive decline than patients with high education in both EOAD and LOAD, the effect was stronger in EOAD, specifically in frontal-executive function. Patients with hypertension showed faster cognitive decline than did patients without hypertension in frontal-executive and general cognitive function in LOAD but not in EOAD. Patients with obesity showed slower decline in general cognitive function than non-obese patients in EOAD but not in LOAD. Conclusions Known risk factors for AD were associated with slower cognitive decline in EOAD but rapid cognitive decline in LOAD.

Vestibular Loss Predicts Poorer Spatial Cognition in Patients with Alzheimer’s Disease

2018 ◽  
Vol 61 (3) ◽  
pp. 995-1003 ◽  
Author(s):  
Eric X. Wei ◽  
Esther S. Oh ◽  
Aisha Harun ◽  
Matthew Ehrenburg ◽  
Yuri Agrawal
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Spatial Cognition ◽  
Vestibular Loss

scholarly journals RALBP1 in Oxidative Stress and Mitochondrial Dysfunction in Alzheimer’s Disease

Cells ◽  
2021 ◽  
Vol 10 (11) ◽  
pp. 3113
Author(s):  
Sanjay Awasthi ◽  
Ashly Hindle ◽  
Neha A. Sawant ◽  
Mathew George ◽  
Murali Vijayan ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cognitive Function ◽  
Mitochondrial Dysfunction ◽  
Mitochondrial Function ◽  
Gene Networks ◽  
Sensory Function ◽  
Expression Of Genes ◽  
The Impact

The purpose of our study is to understand the role of the RALBP1 gene in oxidative stress (OS), mitochondrial dysfunction and cognition in Alzheimer’s disease (AD) pathogenesis. The RALPB1 gene encodes the 76 kDa protein RLIP76 (Rlip). Rlip functions as a stress-responsive/protective transporter of glutathione conjugates (GS-E) and xenobiotic toxins. We hypothesized that Rlip may play an important role in maintaining cognitive function. The aim of this study is to determine whether Rlip deficiency in mice is associated with AD-like cognitive and mitochondrial dysfunction. Brain tissue obtained from cohorts of wildtype (WT) and Rlip+/− mice were analyzed for OS markers, expression of genes that regulate mitochondrial fission/fusion, and synaptic integrity. We also examined mitochondrial ultrastructure in brains obtained from these mice and further analyzed the impact of Rlip deficiency on gene networks of AD, aging, stress response, mitochondrial function, and CREB signaling. Our studies revealed a significant increase in the levels of OS markers and alterations in the expression of genes and proteins involved in mitochondrial biogenesis, dynamics and synapses in brain tissues from these mice. Furthermore, we compared the cognitive function of WT and Rlip+/− mice. Behavioral, basic motor and sensory function tests in Rlip+/− mice revealed cognitive decline, similar to AD. Gene network analysis indicated dysregulation of stress-activated gene expression, mitochondrial function and CREB signaling genes in the Rlip+/− mouse brain. Our results suggest that Rlip deficiency-associated increases in OS and mitochondrial dysfunction could contribute to the development or progression of OS-related AD processes.

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