Alzheimer’s Disease: Physical Activities as an Effective Intervention Tool - A Mini-Review

2019 ◽  
Vol 16 (2) ◽  
pp. 166-171 ◽  
Author(s):  
Blanka Klimova ◽  
Petra Maresova ◽  
Kamil Kuca
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cognitive Decline ◽  
Head Injuries ◽  
Physical Activities ◽  
Scientific Databases ◽  
Slowing Down ◽  
Review Study ◽  
Positive Effect ◽  
Research Studies

Background: There are a few risk factors which definitely have an impact on the development of Alzheimer’s disease (AD). Those include genetics, gender, age, diabetes, head injuries, and lifestyle. Physical activity together with a healthy diet is part of people’s lifestyle. At present, there exist several research studies showing that the physical activities can be a good intervention tool in the delay of cognitive decline in AD. Objective: The aim of this study is to discuss a relationship between the physical activities and the delay and/or maintenance of cognitive decline in AD and the types of physical activities which are especially suitable for this delay. Methods: The method of this review study consists of a method of literature review analysing the data contained in the world’s prestigious scientific databases: PubMed, Springer, Web of Science and Scopus in the period of 2010 - 2015. In addition, a method of comparison of different research studies discussing various aspects and factors of the correlation of physical activities and AD is used. Results: The findings of this review confirm that in most cases, physical activities have a positive effect on the improvement of cognitive decline in AD. Conclusion: Although physical activities seem to be beneficial for people with AD, more convincing results, particularly in the area of specific types of exercises and their impact on slowing down the cognitive decline, respectively AD, are needed.

The effect of exercise interventions on cognitive outcome in Alzheimer's disease: a systematic review

2013 ◽  
Vol 26 (1) ◽  
pp. 9-18 ◽  
Author(s):  
Nicolas Farina ◽  
Jennifer Rusted ◽  
Naji Tabet
Keyword(s):  
Systematic Review ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cognitive Decline ◽  
Controlled Trial ◽  
Meta Analysis ◽  
Cognitive Outcome ◽  
Exercise Interventions ◽  
Slowing Down ◽  
Positive Effect

ABSTRACTBackground:Non-pharmacological interventions may have a role in both the prevention and slowing down of disease progression in Alzheimer's disease (AD). The role of exercise in disease prevention, for example, has been extensively evaluated in large epidemiological studies. Much less is known about the potential benefit of exercise in patients already diagnosed with AD. It was therefore the aim of this systematic review to assess the effectiveness of exercise in attenuating cognitive decline within AD.Method:A systematic review was conducted statistically accompanied by a meta-analysis. Publications between January 1991 and October 2012 were identified by searching the electronic databases PubMed, Science Direct, Web of Knowledge, and PsychINFO. Selected studies required AD patients to take part in an exercise-based randomized controlled trial (RCT) and have a cognitive outcome measure.Results:Six RCTs were identified that exclusively considered the effect of exercise in AD patients. Exercise generally had a positive effect on rate of cognitive decline in AD. A meta-analysis found that exercise interventions have a positive effect on global cognitive function, 0.75 (95% CI = 0.32–1.17).Conclusions:From the six studies reviewed, the evidence suggests that exercise can have a positive effect on rate of cognitive decline in AD. However, the variation between study designs makes conclusions regarding the optimum intervention on cognitive outcome in AD difficult. Well-designed and powered RCTs are still needed to ascertain the efficacy of exercise in slowing down cognitive impairment in AD patients. However, a positive initial indication for exercise efficacy justifies such efforts.

A-5 Examining the Interactive Effects of Traumatic Brain Injury and Apolipoprotein E on Cognitive Decline in Alzheimer’s Disease

2021 ◽  
Vol 36 (6) ◽  
pp. 1044-1044
Author(s):  
Claire Alexander ◽  
Julie Suhr
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cognitive Decline ◽  
Apolipoprotein E ◽  
Negative Impact ◽  
Interactive Effects ◽  
Decline Rate ◽  
History Of ◽  
Positive Effect

Abstract Objective Little research has focused on possible effects of TBI on cognitive decline rate after Alzheimer’s disease (ad) diagnosis. We examined whether Apolipoprotein E (APOE) status and TBI history interact to predict cognitive decline. Method We used data from the National Alzheimer’s Coordinating Centers (N = 463; 42.3% APOE e4 carriers, 7.8% with TBI history, mean baseline age 79.3). Inclusion criteria included normal cognition at baseline with diagnosis of ad at a follow-up visit; baseline age 50 or older; and at least 3 years of follow-up data. Mixed models (random intercept, random slope) were used, with TBI history, APOE status, and their interaction as predictors of interest. Education, race, and history of TIA, stroke, or hypertension were included as covariates. Cognitive measures included mental status exam scores and immediate/delayed story memory. Results After accounting for covariates, TBI history had a positive effect on cognitive decline rate on the screener and immediate memory measures. APOE status did not affect rate of cognitive decline on the screener, but presence of e4 predicted faster decline on immediate and delayed memory. TBI history and APOE status interacted to predict delayed memory decline, such that history of TBI was associated with a reduced rate of decline for e4 non-carriers but there was no effect of TBI for e4 carriers. Conclusion When examining cognitive decline trajectory, TBI history predicted slower decline (a positive effect) while APOE had either a negative impact or no effect, depending on the measure. Future study should examine cognitive decline in the context of demographic and genetic factors.

Subjective Spatial Navigation Complaints - A Frequent Symptom Reported by Patients with Subjective Cognitive Decline, Mild Cognitive Impairment and Alzheimer's Disease

2018 ◽  
Vol 15 (3) ◽  
pp. 219-228 ◽  
Author(s):  
Jiri Cerman ◽  
Ross Andel ◽  
Jan Laczo ◽  
Martin Vyhnalek ◽  
Zuzana Nedelska ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cognitive Impairment ◽  
Mild Cognitive Impairment ◽  
Cognitive Decline ◽  
Spatial Navigation ◽  
Subjective Cognitive Decline ◽  
Great Effort ◽  
Frequent Symptom ◽  
Normal Controls

Background: Great effort has been put into developing simple and feasible tools capable to detect Alzheimer's disease (AD) in its early clinical stage. Spatial navigation impairment occurs very early in AD and is detectable even in the stage of mild cognitive impairment (MCI). Objective: The aim was to describe the frequency of self-reported spatial navigation complaints in patients with subjective cognitive decline (SCD), amnestic and non-amnestic MCI (aMCI, naMCI) and AD dementia and to assess whether a simple questionnaire based on these complaints may be used to detect early AD. Method: In total 184 subjects: patients with aMCI (n=61), naMCI (n=27), SCD (n=63), dementia due to AD (n=20) and normal controls (n=13) were recruited. The subjects underwent neuropsychological examination and were administered a questionnaire addressing spatial navigation complaints. Responses to the 15 items questionnaire were scaled into four categories (no, minor, moderate and major complaints). Results: 55% of patients with aMCI, 64% with naMCI, 68% with SCD and 72% with AD complained about their spatial navigation. 38-61% of these complaints were moderate or major. Only 33% normal controls expressed complaints and none was ranked as moderate or major. The SCD, aMCI and AD dementia patients were more likely to express complaints than normal controls (p's<0.050) after adjusting for age, education, sex, depressive symptoms (OR for SCD=4.00, aMCI=3.90, AD dementia=7.02) or anxiety (OR for SCD=3.59, aMCI=3.64, AD dementia=6.41). Conclusion: Spatial navigation complaints are a frequent symptom not only in AD, but also in SCD and aMCI and can potentially be detected by a simple and inexpensive questionnaire.

Pharmacogenetics of Angiotensin-Converting Enzyme Inhibitors in Patients with Alzheimer's Disease Dementia

2018 ◽  
Vol 15 (4) ◽  
pp. 386-398 ◽  
Author(s):  
Fabricio Ferreira de Oliveira ◽  
Elizabeth Suchi Chen ◽  
Marilia Cardoso Smith ◽  
Paulo Henrique Ferreira Bertolucci
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Angiotensin Converting Enzyme ◽  
Cognitive Decline ◽  
Enzyme Inhibitors ◽  
Late Onset ◽  
Amyloid Β ◽  
Converting Enzyme ◽  
Converting Enzyme Inhibitors ◽  
Alzheimer’S Disease Dementia

Background: While the angiotensin-converting enzyme degrades amyloid-β, angiotensinconverting enzyme inhibitors (ACEis) may slow cognitive decline by way of cholinergic effects, by increasing brain substance P and boosting the activity of neprilysin, and by modulating glucose homeostasis and augmenting the secretion of adipokines to enhance insulin sensitivity in patients with Alzheimer’s disease dementia (AD). We aimed to investigate whether ACE gene polymorphisms rs1800764 and rs4291 are associated with cognitive and functional change in patients with AD, while also taking APOE haplotypes and anti-hypertensive treatment with ACEis into account for stratification. Methods: Consecutive late-onset AD patients were screened with cognitive tests, while their caregivers were queried for functional and caregiver burden scores. Prospective pharmacogenetic correlations were estimated for one year, considering APOE and ACE genotypes and haplotypes, and treatment with ACEis. Results: For 193 patients, minor allele frequencies were 0.497 for rs1800764 – C (44.6% heterozygotes) and 0.345 for rs4291 – T (38.9% heterozygotes), both in Hardy-Weinberg equilibrium. Almost 94% of all patients used cholinesterase inhibitors, while 155 (80.3%) had arterial hypertension, and 124 used ACEis. No functional impacts were found regarding any genotypes or pharmacological treatment. Either for carriers of ACE haplotypes that included rs1800764 – T and rs4291 – A, or for APOE4- carriers of rs1800764 – T or rs4291 – T, ACEis slowed cognitive decline independently of blood pressure variations. APOE4+ carriers were not responsive to treatment with ACEis. Conclusion: ACEis may slow cognitive decline for patients with AD, more remarkably for APOE4- carriers of specific ACE genotypes.

scholarly journals 24(S)-Saringosterol Prevents Cognitive Decline in a Mouse Model for Alzheimer’s Disease

Marine Drugs ◽  
2021 ◽  
Vol 19 (4) ◽  
pp. 190
Author(s):  
Nikita Martens ◽  
Melissa Schepers ◽  
Na Zhan ◽  
Frank Leijten ◽  
Gardi Voortman ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Mouse Model ◽  
Cognitive Decline ◽  
Inflammatory Marker ◽  
Amyloid Β ◽  
Liver Fat ◽  
Gas Chromatography Mass Spectrometry ◽  
Memory Decline ◽  
Plaque Load

We recently found that dietary supplementation with the seaweed Sargassum fusiforme, containing the preferential LXRβ-agonist 24(S)-saringosterol, prevented memory decline and reduced amyloid-β (Aβ) deposition in an Alzheimer’s disease (AD) mouse model without inducing hepatic steatosis. Here, we examined the effects of 24(S)-saringosterol as a food additive on cognition and neuropathology in AD mice. Six-month-old male APPswePS1ΔE9 mice and wildtype C57BL/6J littermates received 24(S)-saringosterol (0.5 mg/25 g body weight/day) (APPswePS1ΔE9 n = 20; C57BL/6J n = 19) or vehicle (APPswePS1ΔE9 n = 17; C57BL/6J n = 19) for 10 weeks. Cognition was assessed using object recognition and object location tasks. Sterols were analyzed by gas chromatography/mass spectrometry, Aβ and inflammatory markers by immunohistochemistry, and gene expression by quantitative real-time PCR. Hepatic lipids were quantified after Oil-Red-O staining. Administration of 24(S)-saringosterol prevented cognitive decline in APPswePS1ΔE9 mice without affecting the Aβ plaque load. Moreover, 24(S)-saringosterol prevented the increase in the inflammatory marker Iba1 in the cortex of APPswePS1ΔE9 mice (p < 0.001). Furthermore, 24(S)-saringosterol did not affect the expression of lipid metabolism-related LXR-response genes in the hippocampus nor the hepatic neutral lipid content. Thus, administration of 24(S)-saringosterol prevented cognitive decline in APPswePS1ΔE9 mice independent of effects on Aβ load and without adverse effects on liver fat content. The anti-inflammatory effects of 24(S)-saringosterol may contribute to the prevention of cognitive decline.

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