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 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 Alzheimer’s Disease and Specialized Pro-Resolving Lipid Mediators: Do MaR1, RvD1, and NPD1 Show Promise for Prevention and Treatment?

2020 ◽  
Vol 21 (16) ◽  
pp. 5783 ◽  
Author(s):  
Keishi Miyazawa ◽  
Hisanori Fukunaga ◽  
Yasuko Tatewaki ◽  
Yumi Takano ◽  
Shuzo Yamamoto ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Lipid Mediators ◽  
Major Contributor ◽  
Resolvin D1 ◽  
The Public ◽  
Aging Society ◽  
Neuroprotectin D1 ◽  
Chronic Neuroinflammation ◽  
Progressive Cognitive Impairment

Alzheimer’s disease (AD) is a common neurodegenerative disease and a major contributor to progressive cognitive impairment in an aging society. As the pathophysiology of AD involves chronic neuroinflammation, the resolution of inflammation and the group of lipid mediators that actively regulate it—i.e., specialized pro-resolving lipid mediators (SPMs)—attracted attention in recent years as therapeutic targets. This review focuses on the following three specific SPMs and summarizes their relationships to AD, as they were shown to effectively address and reduce the risk of AD-related neuroinflammation: maresin 1 (MaR1), resolvin D1 (RvD1), and neuroprotectin D1 (NPD1). These three SPMs are metabolites of docosahexaenoic acid (DHA), which is contained in fish oils and is thus easily available to the public. They are expected to become incorporated into promising avenues for preventing and treating AD in the future.

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 A bacterial cell factory converting glucose into scyllo-inositol, a therapeutic agent for Alzheimer’s disease

2020 ◽  
Vol 3 (1) ◽  
Author(s):  
Christophe Michon ◽  
Choong-Min Kang ◽  
Sophia Karpenko ◽  
Kosei Tanaka ◽  
Shu Ishikawa ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Bacillus Subtilis ◽  
Therapeutic Agent ◽  
Cell Factory ◽  
Inositol Monophosphatase ◽  
Inositol 1 ◽  
Aging Society ◽  
Potential Efficacy ◽  
Artificial Pathway

AbstractA rare stereoisomer of inositol, scyllo-inositol, is a therapeutic agent that has shown potential efficacy in preventing Alzheimer’s disease. Mycobacterium tuberculosis ino1 encoding myo-inositol-1-phosphate (MI1P) synthase (MI1PS) was introduced into Bacillus subtilis to convert glucose-6-phosphate (G6P) into MI1P. We found that inactivation of pbuE elevated intracellular concentrations of NAD+·NADH as an essential cofactor of MI1PS and was required to activate MI1PS. MI1P thus produced was dephosphorylated into myo-inositol by an intrinsic inositol monophosphatase, YktC, which was subsequently isomerized into scyllo-inositol via a previously established artificial pathway involving two inositol dehydrogenases, IolG and IolW. In addition, both glcP and glcK were overexpressed to feed more G6P and accelerate scyllo-inositol production. Consequently, a B. subtilis cell factory was demonstrated to produce 2 g L−1scyllo-inositol from 20 g L−1 glucose. This cell factory provides an inexpensive way to produce scyllo-inositol, which will help us to challenge the growing problem of Alzheimer’s disease in our aging society.

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