Substance Use-Related Cognitive Decline in Families with Autosomal Dominant Alzheimer’s Disease: A Cohort Study

2021 ◽  
pp. 1-17
Author(s):  
Claudia Ramos ◽  
Camilo Villalba ◽  
Jenny García ◽  
Serggio Lanata ◽  
Hugo López ◽  
...  

Background: Cigarette smoking is a known risk factor for Alzheimer’s disease (AD). However, the association between neurodegeneration and other substances has not been fully determined. It is of vital importance to evaluate this relationship in populations at high risk of dementia. Since substance use possibly modifies the progression rate of cognitive decline, we studied this association in a unique and well-phenotyped cohort from the University of Antioquia: carriers of the PSEN1-E280A genetic variant. Objective: To determine the association between substance use and cognitive decline in carriers of the PSEN1-E280A genetic variant. Methods: A retrospective cohort study was conducted with 94 carriers and 69 noncarriers recruited between January 2019 and April 2020. A psychiatrist interviewed the participants using the Consumption of Alcohol, Cigarettes and other Substances questionnaire. The participants were also submitted to cognitive evaluation. The relationship between cognitive decline and substance use was explored through a mixed effects regression model. Results: There was an association between cigarettes and better performance on tasks related to perceptual organization, verbal fluency, and memory in carriers. Alcohol had a positive or negative effect on memory according to the type of alcoholic beverage. Results on marijuana use were no conclusive. Coffee was associated with progressive improvements in executive function and verbal fluency. Conclusion: Cigarette and alcohol were associated with an improvement of some cognitive assessments, possibly by a survival bias. In addition, coffee was related to improvements in executive function and language; therefore, its short-term neuroprotective potential should be studied.

2019 ◽  
Vol 15 ◽  
pp. P701-P701
Author(s):  
Kazushi Suzuki ◽  
Ryoko Ihara ◽  
Takeshi Ikeuchi ◽  
Atsushi Iwata ◽  
Takeshi Iwatsubo

BMJ Open ◽  
2012 ◽  
Vol 2 (1) ◽  
pp. e000380 ◽  
Author(s):  
Zuzana Walker ◽  
Ian McKeith ◽  
Joanne Rodda ◽  
Tarik Qassem ◽  
Klaus Tatsch ◽  
...  

2020 ◽  
Author(s):  
Jin Wang ◽  
Xiaojuan Guo ◽  
Wenhui Lu ◽  
Jie Liu ◽  
Hong Zhang ◽  
...  

Abstract Background:Vascular factors and mitochondria dysfunction contributeto thepathogenesis of Alzheimer’s Disease (AD).DL-3-n-butylphthalide (NBP)has an effect in protecting mitochondria and improving microcirculation. We investigated the effect of NBP in patients with mild-moderate AD already receiving donepezil.Methods: It was a prospective cohort study. 92 mild-moderate AD patients were classified into the donepezil alone group (n=43) or the donepezil combined NBP group (n=49) for 48 weeks. The primary outcome was change of Alzheimer’s disease assessment scale-cognitive subscale (ADAS-cog) from baseline after treatment 48 weeks. All patients were also evaluated with clinician’s interview-based impression of change plus caregiver input (CIBIC-plus), Alzheimer's disease cooperative study-activities of daily living (ADCS-ADL) and neuropsychiatric inventory (NPI) every 12 weeks. All patients were monitored for adverse events (AEs). The efficacy was analyzed using logistic regression analysis.Results:The univariate analysis showed that age wasolder in donepezil alone group(P=0.005), prevalence of hypertension was higher in donepezil alone group(P=0.026).The ADAS-cog score change from baseline in thedonepezil alone group was significant than that in the donepezil combined NBP group at 48 weeks(1.82±5.20 vs -0.38±4.46, P=0.048). The multivariate logistic regression analysis showed that between the 2 groups, there were significant differencesin changes on the ADAS-cog(OR=0.879,95% CI:[0.785,0.984],P=0.026),MMSE(OR=1.270,95% CI:[1.036,1.557],P=0.021), and ADCS-ADL(OR=1.067,95% CI:[1.002,1.136],P=0.042) but no significant differences for changes on the NPI(OR=0.955,95% CI:[0.901,1.013],P=0.125)and CIBIC-plus (OR=0.356,95% CI:[0.093,1.364],P=0.132). The occurrence of AEs was similar in the 2 groups.Conclusions:Over the 48-week treatment period, donepezil combined NBP group had slower cognitive decline and better activities of daily living in patients with mild to moderate AD. These indicated that the multi-target therapeutic effect of NBP may be a new choice for AD treatment.Trial registration:Clinical trial registration URL:https://clinicaltrials.gov/ct2/show/NCT02711683?term=NCT02711683&draw=2&rank=1ClinicalTrials.gov Identifier: NCT02711683. Date of registration: March 14,2016.


2020 ◽  
Author(s):  
Andras Horvath ◽  
Dalida Berente ◽  
Anita Kamondi

Abstract Introduction: In the diagnosis of Alzheimer’s disease (AD), examining memory is predominant. Our aim was to analyse the potential role of various cognitive domains in the cognitive evaluation of AD. Methods: 52 individuals with AD underwent neuropsychological evaluation including Addenbrooke’s Cognitive Examination (ACE). Patients were selected in three groups based on disease duration in years (y) (Group 1: ≤2y n=15; Group 2: 2-4y n=26, Group 3: ≥4y n=11). Covariance weighted intergroup comparison was performed on global cognitive score and subscores of cognitive domains. Spearman’s rho was applied to study the correlation between cognitive subscores and disease duration. Results: Significant difference was found between ACE total scores among groups (χ2=16,03 p<0,001) with a high negative correlation (r= -0,54 p<0,001). With longer disease duration the visuospatial and memory subscores of ACE significantly decreased (χ2=28,36 p<0,001; and f=12,05 p<0,001 respectively). In the early phase of cognitive decline verbal fluency and memory were equally impaired (p>0.05). Visuospatial score showed strong negative correlation with disease duration (r:-0.73).Conclusion: Impairment of verbal fluency seems to have similar diagnostic potential in the early identification of Alzheimer’s disease as memory decline. Visuospatial assessment might be a good marker to monitor the progression of cognitive decline.


2014 ◽  
Vol 10 ◽  
pp. P566-P567
Author(s):  
Rena Muraoka ◽  
Mayumi Saito ◽  
Tomomi Shinoda ◽  
Yuichi Satoh ◽  
Tetsuya Maeda ◽  
...  

2016 ◽  
Vol 67 (655) ◽  
pp. e111-e117 ◽  
Author(s):  
Markus Bleckwenn ◽  
Luca Kleineidam ◽  
Michael Wagner ◽  
Frank Jessen ◽  
Siegfried Weyerer ◽  
...  

BackgroundArteriosclerotic disorders increase the risk of dementia. As they have common causes and risk factors, coronary heart disease (CHD) could influence the course of dementia.AimTo determine whether CHD increases the speed of cognitive decline in Alzheimer’s disease, and to discuss the potential for secondary cardiovascular prevention to modify this decline.Design and settingProspective multicentre cohort study in general practices in six cities in Germany.MethodParticipants were patients with probable mild-to-moderate Alzheimer’s dementia or mixed dementia (n = 118; mean age 85.6 [±3.4] years, range 80–96 years). The authors assessed the presence of CHD according to the family physicians’ diagnosis. Cognitive performance was measured during home visits for up to 3 years in intervals of 6 months, using Mini Mental State Examination (MMSE) and Clinical Dementia Rating Sum of Boxes (CDR-SoB). The authors also recorded whether patients died in the observation period.ResultsAt baseline, 65 patients (55%) had CHD and/or a heart condition following a myocardial infarction. The presence of CHD accelerated cognitive decline (MMSE, P<0.05) by about 66%, and reduced cognitive-functional ability (CDR-SoB, P<0.05) by about 83%, but had no impact on survival.ConclusionThe study shows that CHD has a significant influence on cognitive decline in older patients with late-onset dementia. The dementia process might therefore be positively influenced by cardiovascular prevention, and this possible effect should be further investigated.


2014 ◽  
Vol 35 (10) ◽  
pp. 2422.e3-2422.e8 ◽  
Author(s):  
Hongsheng Gui ◽  
Chao Qiang Jiang ◽  
Stacey S. Cherny ◽  
Pak Chung Sham ◽  
Lin Xu ◽  
...  

2019 ◽  
Author(s):  
A. Shepherd ◽  
J.K.H. Lim ◽  
V.H.Y. Wong ◽  
A.M. Zeleznikow-Johnston ◽  
L. Churilov ◽  
...  

AbstractExecutive function deficits in Alzheimer’s disease (AD) occur early in disease progression and may be predictive of cognitive decline. However, no preclinical studies have identified deficits in rewarded executive function in the commonly used APP/PS1 mouse model. To address this, we assessed 12-26 month old APP/PS1 mice on rewarded reversal and/or extinction tasks. 16-month-old, but not 13- or 26-month-old, APP/PS1 mice showed an attenuated rate of extinction. Reversal deficits were seen in 22-month-old, but not 13-month-old APP/PS1 animals. We then confirmed that impairments in reversal were unrelated to previously reported visual impairments in both AD mouse models and humans. Age, but not genotype, had a significant effect on markers of retinal health, indicating the deficits seen in APP/PS1 mice were directly related to cognition. This is the first characterisation of rewarded executive function in APP/PS1 mice, and has great potential to facilitate translation from preclinical models to the clinic.


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