Towards a Consensus on Alzheimer’s Disease Comorbidity?

Avitan, Iska; Halperin, Y.; Saha, Trishna; Bloch, Naamah; Atrahimovich, Dana; Polis, Baruh; Samson, Abraham O.; Braitbard, Ori

doi:10.3390/jcm10194360

Cited by 29 publications

(21 citation statements)

References 64 publications

(87 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Several studies have linked the upregulation of arginase to a variety of other central nervous system diseases, including Parkinson's disease [14]. A recent study investigating comorbid Alzheimer's disease found that Alzheimer's disease is strongly associated with Parkinson's disease [15].…”

Section: Discussionmentioning

confidence: 99%

Plasma Caffeine Levels and Risk of Alzheimer’s Disease and Parkinson’s Disease: Mendelian Randomization Study

Larsson

Woolf

2022

Nutrients

View full text Add to dashboard Cite

We leveraged genetic variants associated with caffeine metabolism in the two-sample Mendelian randomization framework to investigate the effect of plasma caffeine levels on the risk of Alzheimer’s disease and Parkinson’s disease. Genetic association estimates for the outcomes were obtained from the International Genomics of Alzheimer’s Project, the International Parkinson’s Disease Genomics consortium, the FinnGen consortium, and the UK Biobank. Genetically predicted higher plasma caffeine levels were associated with a non-significant lower risk of Alzheimer’s disease (odds ratio 0.87; 95% confidence interval 0.76, 1.00; p = 0.056). A suggestive association was observed for genetically predicted higher plasma caffeine levels and lower risk of Parkinson’s disease in the FinnGen consortium. but not in the International Parkinson’s Disease Genomics consortium; no overall association was found (odds ratio 0.92; 95% confidence interval 0.77, 1.10; p = 0.347). This study found possible suggestive evidence of a protective role of caffeine in Alzheimer’s disease. The association between caffeine and Parkinson’s disease requires further study.

show abstract

Section: Discussionmentioning

confidence: 99%

Plasma Caffeine Levels and Risk of Alzheimer’s Disease and Parkinson’s Disease: Mendelian Randomization Study

Larsson

Woolf

2022

Nutrients

View full text Add to dashboard Cite

show abstract

“…It is the predominant type of dementia across the world, accounting for approximately 70% of all cases, and is one of the leading causes of death globally . Recent studies have reported AD development to be a comorbidity with other pathologies, including type 2 diabetes, obesity, and cardiovascular disease . There is also an increased risk of metabolic syndrome, which has been observed in both human population-based surveys and AD-related mice models. , Patients with AD demonstrate a deregulation in insulin signaling, leading to the identification of AD as type 3 diabetes .…”

Section: Introductionmentioning

confidence: 99%

Helicobacter pylori and Alzheimer’s Disease-Related Metabolic Dysfunction: Activation of TLR4/Myd88 Inflammation Pathway from p53 Perspective and a Case Study of Low-Dose Radiation Intervention

Zhao

Shen

Zhou

et al. 2022

ACS Chem. Neurosci.

View full text Add to dashboard Cite

Gut dysbiosis is observed in Alzheimer's disease (AD) and is frequently associated with AD-induced metabolic dysfunction. However, the extent and specific underlying molecular mechanisms triggered by alterations of gut microbiota composition and function mediating ADinduced metabolic dysfunction in AD remain incompletely uncovered. Here, we indicate that Helicobacter pylori (H. pylori) is abundant in AD patients with relative metabolic dysfunction. Fecal microbiota transplantation from the AD patients promoted metabolic dysfunction in mice and increased gut permeability. H. pylori increased gut permeability through activation of the TLR4/Myd88 inflammation pathway in a p53-dependent manner, leading to metabolic dysfunction. Moreover, p53 deficiency reduced bile acid concentration, leading to an increased abundance of H. pylori colonization. Overall, these data identify H. pylori as a key promoter of ADinduced metabolic dysfunction.

show abstract

“…AD is the most common neurodegenerative disease in the elderly with complex etiologies, and its incidence is increasing due to longer life expectancy [ 1 ]. A growing literature confirms that chronic obesity, high cholesterol, high blood pressure, and diabetes are important factors inducing memory loss and impaired cognition [ 43 ]. Each of the risk factors increases the memory dysfunction risk by approximately twofold.…”

Section: Discussionmentioning

confidence: 99%

Mitigation of Memory Impairment with Fermented Fucoidan and λ-Carrageenan Supplementation through Modulating the Gut Microbiota and Their Metagenome Function in Hippocampal Amyloid-β Infused Rats

Zhang

et al. 2022

Cells

View full text Add to dashboard Cite

Attenuating acetylcholinesterase and insulin/insulin-like growth factor-1 signaling in the hippocampus is associated with Alzheimer’s disease (AD) development. Fucoidan and carrageenan are brown and red algae, respectively, with potent antibacterial, anti-inflammatory, antioxidant and antiviral activities. This study examined how low-molecular-weight (MW) and high-MW fucoidan and λ-carrageenan would improve memory impairment in Alzheimer’s disease-induced rats caused by an infusion of toxic amyloid-β(Aβ). Fucoidan and λ-carrageenan were dissected into low-MW by Luteolibacter algae and Pseudoalteromonas carrageenovora. Rats receiving an Aβ(25–35) infusion in the CA1 region of the hippocampus were fed dextrin (AD-Con), 1% high-MW fucoidan (AD-F-H), 1% low-MW fucoidan (AD-F-L), 1% high-MW λ-carrageenan (AD-C-H), and 1% low-MW λ-carrageenan (AD-C-L) for six weeks. Rats to receive saline infusion (Normal-Con) had an AD-Con diet. The AD-F-L group showed an improved memory function, which manifested as an enhanced Y-maze spontaneous alternation test, water maze, and passive avoidance tests, similar to the Normal-Con group. AD-F-L also potentiated hippocampal insulin signaling and increased the expression of ciliary neurotrophic factor (CNTF) and brain-derived neurotrophic factor (BDNF) in the hippocampus. AD-C-L improved the memory function mainly by increasing the BDNF content. AD-F-H and AD-C-H did not improve the memory function. Compared to AD-Con, the ascending order of AD-C-H, AD-F-H, AD-C-L, and AD-F-L increased insulin signaling by enhancing the pSTAT3®pAkt®pGSK-3β pathway. AD-F-L improved glucose tolerance the most. Compared to AD-CON, the AD-F-L treatment increased the serum acetate concentrations and compensated for the defect of cerebral glucose metabolism. AD-Con increased Clostridium, Terrisporobacter and Sporofaciens compared to Normal-Con, and AD-F-L and AD-C-L increased Akkermentia. In conclusion, AD-F-L and AD-C-L alleviated the memory function in the rats with induced AD symptoms by modulating.

show abstract

Towards a Consensus on Alzheimer’s Disease Comorbidity?

Cited by 29 publications

References 64 publications

Plasma Caffeine Levels and Risk of Alzheimer’s Disease and Parkinson’s Disease: Mendelian Randomization Study

Plasma Caffeine Levels and Risk of Alzheimer’s Disease and Parkinson’s Disease: Mendelian Randomization Study

Helicobacter pylori and Alzheimer’s Disease-Related Metabolic Dysfunction: Activation of TLR4/Myd88 Inflammation Pathway from p53 Perspective and a Case Study of Low-Dose Radiation Intervention

Mitigation of Memory Impairment with Fermented Fucoidan and λ-Carrageenan Supplementation through Modulating the Gut Microbiota and Their Metagenome Function in Hippocampal Amyloid-β Infused Rats

Contact Info

Product

Resources

About