scholarly journals P1-345: Role of Vitamin D Signaling in Sporadic Alzheimer’s Disease: A Clinico-Experimental Study

2016 ◽  
Vol 12 ◽  
pp. P561-P562
Author(s):  
Anindita Banerjee ◽  
Vineet Kumar Khemka ◽  
Debashree Roy ◽  
Aparajita Dhar ◽  
Tapan Kumar Sinha Roy ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Experimental Study ◽  
Vitamin D ◽  
Sporadic Alzheimer’S Disease ◽  
Vitamin D Signaling

The Role of Microglia in Sporadic Alzheimer’s Disease

2021 ◽  
Vol 79 (3) ◽  
pp. 961-968
Author(s):  
Wolfgang J. Streit ◽  
Habibeh Khoshbouei ◽  
Ingo Bechmann
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Late Onset ◽  
Genetic Mutations ◽  
Sporadic Alzheimer’S Disease ◽  
Immune Effector ◽  
Effector Cells ◽  
Immune Effector Cells ◽  
Amyloid Cascade

Microglia constitute the brain’s immune system and their involvement in Alzheimer’s disease has been discussed. Commonly, and in line with the amyloid/neuroinflammation cascade hypothesis, microglia have been portrayed as potentially dangerous immune effector cells thought to be overactivated by amyloid and producing neurotoxic inflammatory mediators that lead to neurofibrillary degeneration. We disagree with this theory and offer as an alternative the microglial dysfunction theory stating that microglia become impaired in their normally neuroprotective roles because of aging, i.e., they become senescent and aging neurons degenerate because they lack the needed microglial support for their survival. Thus, while the amyloid cascade theory relies primarily on genetic data, the dysfunction theory incorporates aging as a critical etiological factor. Aging is the greatest risk factor for the sporadic (late-onset) and most common form of Alzheimer’s disease, where fully penetrant genetic mutations are absent. In this review, we lay out and discuss the human evidence that supports senescent microglial dysfunction and conflicts with the amyloid/neuroinflammation idea.

The modulatory role of phloretin in Aβ25–35 induced sporadic Alzheimer’s disease in rat model

2018 ◽  
Vol 392 (3) ◽  
pp. 327-339 ◽  
Author(s):  
Priya J. Ghumatkar ◽  
Sachin P. Patil ◽  
Vaibhavi Peshattiwar ◽  
Tushara Vijaykumar ◽  
Vikas Dighe ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Rat Model ◽  
Sporadic Alzheimer’S Disease

P1-046: ROLE OF PLD3 RARE VARIANTS IN EUROPEAN SPORADIC ALZHEIMER'S DISEASE PATIENTS

2014 ◽  
Vol 10 ◽  
pp. P319-P320
Author(s):  
Alfredo Ramirez ◽  
Stefanie Heilmann ◽  
Dmitriy Drichel ◽  
Isabel Hernandez ◽  
Alberto Lleó ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Rare Variants ◽  
Sporadic Alzheimer’S Disease

P2-244: THE CORRELATION BETWEEN CSF AMYLOID BETA 1-42 LEVELS AND CSF VITAMIN D (25OHD) LEVELS IN PATIENTS WITH SPORADIC ALZHEIMER'S DISEASE

2006 ◽  
Vol 14 (7S_Part_14) ◽  
pp. P766-P766
Author(s):  
Erdinc Dursun ◽  
Merve Alaylıoğlu ◽  
Irem L. Atasoy ◽  
Busra Sengul ◽  
Ezgi Soncu Buyukiscan ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Vitamin D ◽  
Amyloid Beta ◽  
Sporadic Alzheimer’S Disease

scholarly journals P4-259: White matter hyperintensities in Alzheimer's disease: The potential protective role of vitamin D

2013 ◽  
Vol 9 ◽  
pp. P800-P800
Author(s):  
Cedric Annweiler ◽  
Manuel Montero-Odasso ◽  
Robert Bartha ◽  
Olivier Beauchet
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Vitamin D ◽  
White Matter ◽  
White Matter Hyperintensities ◽  
Protective Role

scholarly journals The Role of BMI1 in Late-Onset Sporadic Alzheimer’s Disease

Genes ◽  
2020 ◽  
Vol 11 (7) ◽  
pp. 825
Author(s):  
Ryan Hogan ◽  
Anthony Flamier ◽  
Eleonora Nardini ◽  
Gilbert Bernier
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Early Onset ◽  
Late Onset ◽  
Single Gene ◽  
Short Review ◽  
Sporadic Alzheimer’S Disease ◽  
Mendelian Genetics ◽  
Bmi1 Expression

Late-onset sporadic Alzheimer’s disease (LOAD) seems to contain a “hidden” component that cannot be explained by classical Mendelian genetics, with advanced aging being the strongest risk factor. More surprisingly, whole genome sequencing analyses of early-onset sporadic Alzheimer’s disease cohorts also revealed that most patients do not present classical disease-associated variants or mutations. In this short review, we propose that BMI1 is possibly epigenetically silenced in LOAD. Reduced BMI1 expression is unique to LOAD compared to familial early-onset AD (EOAD) and other related neurodegenerative disorders; moreover, reduced expression of this single gene is sufficient to reproduce most LOAD pathologies in cellular and animal models. We also show the apparent amyloid and Tau-independent nature of this epigenetic alteration of BMI1 expression. Lastly, examples of the mechanisms underlying epigenetic dysregulation of other LOAD-related genes are also illustrated.

Liver-Brain Axis in Sporadic Alzheimer’s Disease: Role of Ten Signature Genes in a Mouse model

2020 ◽  
Vol 19 ◽  
Author(s):  
Ruchi Jakhmola-Mani ◽  
Anam Islam ◽  
Deepshikha Pande Katare
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cholesterol Biosynthesis ◽  
Brain Diseases ◽  
Entire Body ◽  
Junk Food ◽  
Acid Modification ◽  
Sporadic Alzheimer’S Disease ◽  
Nutritional Effect

Aim:: Poor nutritional effect of junk food induces injurious adversities to the liver and brain but still most of the developing nations survives on these diets to compensate for fast-paced lifestyle. Aim of the study is to infer the proteinconnections behind liver-brain axis and identify the role of these proteins in causing neurodegenerative disorders. Background: : Chronic consumption of fructose and fat rich food works as a toxin in body and have the ability to cause negative metabolic shift. Recently a study was published in Annals of Internal Medicine (2019) citing the loss of vision and hearing in a 14-year-old boy whose diet was strictly restricted to fries and junk-food for almost a decade. This puts the entire body on insulin resistance and related co-morbidities and causes simultaneous damaging effects in liver as well brain. This work provides insights into liver-brain axis and explains how liver is involved in brain related disorders. Objective: : In this study transcriptomic data relating to chronic eating of junk-food was analyzed and simultaneous damage that happens in liver and brain was assessed at molecular level. Method:: Transcriptomic study was taken from GEO database and analysed to find out the genes dysregulated in both liver and brain during this metabolic stress. Cytoscapev3.7 was used to decipher the signalling between liver and brain. This connection between both was called as Liver-Brain axis. Results : The results obtained from our study indicates the role of TUBB5-HYOU1-SDF2L1-DECR1-CDH1-EGFR-SKP2- SOD1-IRAK1-FOXO1 gene signature towards the decline of concurrent liver and brain health. Dysregulated levels of these genes are linked to molecular processes like cellular senescence, hypoxia, glutathione synthesis, amino acid modification, increased nitrogen content, synthesis of BCAAs, cholesterol biosynthesis, steroid hormone signalling and VEGF pathway. Conclusion: We strongly advocate that prolonged consumption of junk food is a major culprit in brain related disorders like Alzheimer’s disease and propose that receptors for brain diseases lie outside the brain and aiming them for drug discovery and design may be beneficial in future clinical studies. This study also discusses the connection between NAFLD (nonalcoholic fatty liver disease) and sAD (sporadic Alzheimer’s disease) owing to liver-brain axis.

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