[P1-451]: MEASURING SYNTHETIC AGE VIA MORPHOMETRY AS A PROXY OF BRAIN HEALTH IN INDIVIDUALS WITH CLINICAL ALZHEIMER'S DISEASE

2017 ◽  
Vol 13 (7S_Part_9) ◽  
pp. P458-P459
Author(s):  
Olivier Potvin ◽  
Louis Dieumegarde ◽  
Simon Duchesne
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Brain Health

scholarly journals Big data to smart data in Alzheimer's disease: The brain health modeling initiative to foster actionable knowledge

2016 ◽  
Vol 12 (9) ◽  
pp. 1014-1021 ◽  
Author(s):  
Hugo Geerts ◽  
Penny A. Dacks ◽  
Viswanath Devanarayan ◽  
Magali Haas ◽  
Zaven S. Khachaturian ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Big Data ◽  
Brain Health ◽  
Actionable Knowledge ◽  
Smart Data ◽  
The Brain

Lactobacillus probiotics improved the gut microbiota profile of a Drosophila melanogaster Alzheimer’s disease model and alleviated neurodegeneration in the eye

2020 ◽  
Vol 11 (1) ◽  
pp. 79-89 ◽  
Author(s):  
F.H.P. Tan ◽  
G. Liu ◽  
S.-Y.A. Lau ◽  
M.H. Jaafar ◽  
Y.-H. Park ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Drosophila Melanogaster ◽  
Gut Microbiota ◽  
Neurodegenerative Disorders ◽  
Dietary Intervention ◽  
Disease Model ◽  
Brain Health ◽  
Potential Biomarker ◽  
Microbiota Diversity

Alzheimer’s disease (AD) is a progressive disease and one of the most common forms of neurodegenerative disorders. Emerging evidence is supporting the use of various strategies that modulate gut microbiota to exert neurological and psychological changes. This includes the utilisation of probiotics as a natural and dietary intervention for brain health. Here, we showed the potential AD-reversal effects of Lactobacillus probiotics through feeding to our Drosophila melanogaster AD model. The administration of Lactobacillus strains was able to rescue the rough eye phenotype (REP) seen in AD-induced Drosophila, with a more prominent effect observed upon the administration of Lactobacillus plantarum DR7 (DR7). Furthermore, we analysed the gut microbiota of the AD-induced Drosophila and found elevated levels of Wolbachia. The administration of DR7 restored the gut microbiota diversity of AD-induced Drosophila with a significant reduction in Wolbachia’s relative abundance, accompanied by an increase of Stenotrophomonas and Acetobacter. Through functional predictive analyses, Wolbachia was predicted to be positively correlated with neurodegenerative disorders, such as Parkinson’s, Huntington’s and Alzheimer’s diseases, while Stenotrophomonas was negatively correlated with these neurodegenerative disorders. Altogether, our data exhibited DR7’s ability to ameliorate the AD effects in our AD-induced Drosophila. Thus, we propose that Wolbachia be used as a potential biomarker for AD.

scholarly journals Reducing the Risk of Alzheimer’s Disease and Maintaining Brain Health in an Aging Society

2018 ◽  
Vol 133 (3) ◽  
pp. 225-229 ◽  
Author(s):  
Melinda Kelley ◽  
Brigette Ulin ◽  
Lisa C. McGuire
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Brain Health ◽  
Aging Society

scholarly journals Neuropathological correlates and genetic architecture of microglial activation in elderly human brain

2018 ◽  
Author(s):  
Daniel Felsky ◽  
Tina Roostaei ◽  
Kwangsik Nho ◽  
Shannon L. Risacher ◽  
Elizabeth M. Bradshaw ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Human Brain ◽  
Cognitive Decline ◽  
Genetic Architecture ◽  
Microglial Activation ◽  
Brain Health ◽  
Positron Emission ◽  
Genome Wide

AbstractMicroglia, the resident immune cells of the brain, have important roles in brain health. However, little is known about the regulation and consequences of microglial activation in the aging human brain. We assessed the effect of microglial activation in the aging human brain by calculating the proportion of activated microglia (PAM), based on morphologically defined stages of activation in four regions sampled postmortem from up to 225 elderly individuals. We found that cortical and not subcortical PAM measures were strongly associated with β-amyloid, tau-related neuropathology, and rates of cognitive decline. Effect sizes for PAM measures are substantial, comparable to that of APOE ɛ4, the strongest genetic risk factor for Alzheimer’s disease. Mediation modeling suggests that PAM accelerates accumulation of tau pathology leading to cognitive decline, supporting an upstream role for microglial activation in Alzheimer’s disease. Genome-wide analyses identified a common variant (rs2997325) influencing cortical PAM that also affected in vivo microglial activation measured by positron emission tomography using [11C]-PBR28 in an independent cohort. Finally, we identify overlaps of PAM’s genetic architecture with those of Alzheimer’s disease, educational attainment, and several other traits.

scholarly journals The Effectiveness of Vitamin E Treatment in Alzheimer’s Disease

2019 ◽  
Vol 20 (4) ◽  
pp. 879 ◽  
Author(s):  
Ana Lloret ◽  
Daniel Esteve ◽  
Paloma Monllor ◽  
Ana Cervera-Ferri ◽  
Angeles Lloret
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Vitamin E ◽  
Brain Health ◽  
Beneficial Effects ◽  
Limited Effectiveness ◽  
Anti Inflammatory ◽  
Positive Results

Vitamin E was proposed as treatment for Alzheimer’s disease many years ago. However, the effectiveness of the drug is not clear. Vitamin E is an antioxidant and neuroprotector and it has anti-inflammatory and hypocholesterolemic properties, driving to its importance for brain health. Moreover, the levels of vitamin E in Alzheimer’s disease patients are lower than in non-demented controls. Thus, vitamin E could be a good candidate to have beneficial effects against Alzheimer’s. However, evidence is consistent with a limited effectiveness of vitamin E in slowing progression of dementia; the information is mixed and inconclusive. The question is why does vitamin E fail to treat Alzheimer’s disease? In this paper we review the studies with and without positive results in Alzheimer’s disease and we discuss the reasons why vitamin E as treatment sometimes has positive results on cognition but at others, it does not.

scholarly journals Anxiety as a risk factor of Alzheimer's disease and vascular dementia

2018 ◽  
Vol 213 (5) ◽  
pp. 654-660 ◽  
Author(s):  
Eva Becker ◽  
Claudia Lorena Orellana Rios ◽  
Claas Lahmann ◽  
Gerta Rücker ◽  
Joachim Bauer ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Risk Factor ◽  
Vascular Dementia ◽  
Functional Relation ◽  
Hazard Ratio ◽  
Brain Health ◽  
Future Studies ◽  
Prognostic Effect

BackgroundThe aetiology of dementia is not yet fully understood. Stress can have a damaging effect on brain health. The prognostic effect of anxiety is still unclear regarding Alzheimer's disease as well as vascular dementia.AimsTo explore the association between anxiety and future dementia.MethodMedline, PsycINFO, CINAHL, Web of Science and ALOIS were searched for publications up to 12 January 2018. Longitudinal studies with a follow-up of at least 2 years were included, if the trait or state anxiety had been assessed at baseline. Studies with cognitive impairment at baseline were not included. We used a random effects model to calculate the pooled time to Alzheimer's disease and incidence of vascular dementia.ResultsAnxiety predicts risk of Alzheimer's disease (n = 26 193 out of seven studies, hazard ratio1.53, 95% CI 1.16–2.01, P < 0.01) and vascular dementia (n = 4916 out of two studies, odds ratio1.88, 95% CI 1.05–3.36, P < 0.01). The pooled hazard ratio regarding risk of Alzheimer's disease was still significant when excluding studies with critical risk of bias (n = 14 110 out of six studies, hazard ratio 1.35, 95% CI 1.08–1.70, P < 0.01).ConclusionsAnxiety is a risk factor for both types of dementia. The temporal and functional relation between anxiety and dementia needs investigation in future studies. The protective value of treating anxiety should be explored further.Declaration of interestNone.

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