scholarly journals Dietary Spray-Dried Porcine Plasma Reduces Neuropathological Alzheimer’s Disease Hallmarks in SAMP8 Mice

Nutrients ◽  
2021 ◽  
Vol 13 (7) ◽  
pp. 2369
Author(s):  
Cristina Rosell-Cardona ◽  
Christian Griñan-Ferré ◽  
Anna Pérez-Bosque ◽  
Javier Polo ◽  
Mercè Pallàs ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Control Diet ◽  
Dietary Supplementation ◽  
Activation Markers ◽  
Effects Of Aging ◽  
Samp8 Mice ◽  
Spray Dried ◽  
Gene Expression Levels ◽  
Pro Inflammatory Cytokines

Alzheimer’s disease (AD) is characterized by the aberrant processing of amyloid precursor protein (APP) and the accumulation of hyperphosphorylated tau, both of which are accompanied by neuroinflammation. Dietary supplementation with spray-dried porcine plasma (SDP) has anti-inflammatory effects in inflammation models. We investigated whether dietary supplementation with SDP prevents the neuropathological features of AD. The experiments were performed in 2- and 6-month-old SAMP8 mice fed a control diet, or a diet supplemented with 8% SDP, for 4 months. AD brain molecular markers were determined by Western blot and real-time PCR. Senescent mice showed reduced levels of p-GSK3β (Ser9) and an increase in p-CDK5, p-tau (Ser396), sAPPβ, and the concentration of Aβ40, (all p < 0.05). SDP prevented these effects of aging and reduced Bace1 levels (all p < 0.05). Senescence increased the expression of Mme1 and Ide1 and pro-inflammatory cytokines (Il-17 and Il-18; all p < 0.05); these changes were prevented by SDP supplementation. Moreover, SDP increased Tgf-β expression (p < 0.05). Furthermore, in aged mice, the gene expression levels of the microglial activation markers Trem2, Ym1, and Arg1 were increased, and SDP prevented these increases (all p < 0.05). Thus, dietary SDP might delay AD onset by reducing its hallmarks in senescent mice.

scholarly journals Reply to Nifli, A.-P. Comment on “Rosell-Cardona et al. Dietary Spray-Dried Porcine Plasma Reduces Neuropathological Alzheimer’s Disease Hallmarks in SAMP8 Mice. Nutrients 2021, 13, 2369”

Nutrients ◽  
2021 ◽  
Vol 13 (11) ◽  
pp. 4065
Author(s):  
Cristina Rosell-Cardona ◽  
Christian Griñan-Ferré ◽  
Anna Pérez-Bosque ◽  
Javier Polo ◽  
Mercè Pallàs ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Recent Work ◽  
Samp8 Mice ◽  
Spray Dried

Thank you for your comments on our recent work of the effects of supplementation with spray-dried porcine plasma (SDP) on neuropathological markers of Alzheimer’s disease (AD) [...]

scholarly journals Comment on Rosell-Cardona et al. Dietary Spray-Dried Porcine Plasma Reduces Neuropathological Alzheimer’s Disease Hallmarks in SAMP8 Mice. Nutrients 2021, 13, 2369

Nutrients ◽  
2021 ◽  
Vol 13 (11) ◽  
pp. 4053
Author(s):  
Artemissia-Phoebe Nifli
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Dementia Risk ◽  
Samp8 Mice ◽  
Spray Dried

Interventions focusing on dementia risk and/or dementia modification in association with senescence are essential, given the unfavourable demographics [...]

scholarly journals Chronic Dietary Supplementation of 4% Figs on the Modification of Oxidative Stress in Alzheimer’s Disease Transgenic Mouse Model

2014 ◽  
Vol 2014 ◽  
pp. 1-8 ◽  
Author(s):  
Selvaraju Subash ◽  
Musthafa Mohamed Essa ◽  
Abdullah Al-Asmi ◽  
Samir Al-Adawi ◽  
Ragini Vaishnav
Keyword(s):  
Oxidative Stress ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Antioxidant Status ◽  
Control Diet ◽  
Dietary Supplementation ◽  
Learning Ability ◽  
Protein Carbonyls ◽  
Membrane Bound ◽  
Membrane Bound Enzymes

We assessed the changes in the plasma Aβ, oxidative stress/antioxidants, and membrane bound enzymes in the cerebral cortex and hippocampus of Alzheimer’s disease (AD) transgenic mice (Tg2576) after dietary supplementation of Omani figs fruits for 15 months along with spatial memory and learning test. AD Tg mice on control diet without figs showed significant impairment in spatial learning ability compared to the wild-type mice on same diet and figs fed Tg mice as well. Significant increase in oxidative stress and reduced antioxidant status were observed in AD Tg mice. 4% figs treated AD Tg mice significantly attenuated oxidative damage, as evident by decreased lipid peroxidation and protein carbonyls and restoration of antioxidant status. Altered activities of membrane bound enzymes (Na+K+ATPase and acetylcholinesterase (AChE)) in AD Tg mice brain regions and was restored by figs treatment. Further, figs supplementation might be able to decrease the plasma levels of Aβ(1–40, 1–42) significantly in Tg mice suggesting a putative delay in the formation of plaques, which might be due to the presence of high natural antioxidants in figs. But this study warrants further extensive investigation to find a novel lead for a therapeutic target for AD from figs.

scholarly journals Musical Electroacupuncture May Be a Better Choice than Electroacupuncture in a Mouse Model of Alzheimer’s Disease

2016 ◽  
Vol 2016 ◽  
pp. 1-9 ◽  
Author(s):  
Jing Jiang ◽  
Gang Liu ◽  
Suhua Shi ◽  
Zhigang Li
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Mouse Model ◽  
Frontal Lobe ◽  
Morris Water Maze ◽  
Water Maze ◽  
Morris Water Maze Test ◽  
Maze Test ◽  
Model Of Alzheimer’S Disease ◽  
Samp8 Mice

Objectives. To compare musical electroacupuncture and electroacupuncture in a mouse model of Alzheimer’s disease.Methods. In this study, 7.5-month-old male senescence-accelerated mouse prone 8 (SAMP8) mice were used as an Alzheimer’s disease animal model. In the normal control paradigm, 7.5-month-old male SAMR1 mice were used as the blank control group (N group). After 15 days of treatment, using Morris water maze test, micro-PET, and immunohistochemistry, the differences among the musical electroacupuncture (MEA), electroacupuncture (EA), Alzheimer’s disease (AD), and normal (N) groups were assessed.Results. The Morris water maze test, micro-PET, and immunohistochemistry revealed that MEA and EA therapies could improve spatial learning and memory ability, glucose metabolism level in the brain, and Aβamyloid content in the frontal lobe, compared with the AD group (P<0.05). Moreover, MEA therapy performed better than EA treatment in decreasing amyloid-beta levels in the frontal lobe of mice with AD.Conclusion. MEA therapy may be superior to EA in treating Alzheimer’s disease as demonstrated in SAMP8 mice.

scholarly journals The Rat Prefrontal-Cortex Transcriptome: Effects of Aging and Sporadic Alzheimer’s Disease–Like Pathology

2018 ◽  
Vol 74 (1) ◽  
pp. 33-43 ◽  
Author(s):  
Natalia A Stefanova ◽  
Nikita I Ershov ◽  
Kseniya Yi Maksimova ◽  
Natalia A Muraleva ◽  
Mikhail A Tyumentsev ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Prefrontal Cortex ◽  
Sporadic Alzheimer’S Disease ◽  
Effects Of Aging

Abnormal platelet amyloid‐β precursor protein metabolism in SAMP8 mice: Evidence for peripheral marker in Alzheimer's disease

2019 ◽  
Vol 234 (12) ◽  
pp. 23528-23536 ◽  
Author(s):  
Lizhi Chen ◽  
Shicheng Xu ◽  
Tong Wu ◽  
Yijia Shao ◽  
Li Luo ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Protein Metabolism ◽  
Amyloid Β ◽  
Precursor Protein ◽  
Samp8 Mice

Comparative Analyses of DHA‐Phosphatidylcholine Forage and Liposomes on Alzheimer's Disease in SAMP8 Mice

2019 ◽  
Vol 121 (5) ◽  
pp. 1800524 ◽  
Author(s):  
Jing Meng ◽  
Miaomiao Zhou ◽  
Chengcheng Wang ◽  
Changhu Xue ◽  
Tiantian Zhang ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Comparative Analyses ◽  
Samp8 Mice

IL12/23 p40 Inhibition Ameliorates Alzheimer's Disease-Associated Neuropathology and Spatial Memory in SAMP8 Mice

2013 ◽  
Vol 38 (3) ◽  
pp. 633-646 ◽  
Author(s):  
Meng-Shan Tan ◽  
Jin-Tai Yu ◽  
Teng Jiang ◽  
Xi-Chen Zhu ◽  
Hua-Shi Guan ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Spatial Memory ◽  
Samp8 Mice

scholarly journals Enhancer variants associated with Alzheimer’s disease affect gene expression via chromatin looping

2019 ◽  
Vol 12 (1) ◽  
Author(s):  
Masataka Kikuchi ◽  
Norikazu Hara ◽  
Mai Hasegawa ◽  
Akinori Miyashita ◽  
Ryozo Kuwano ◽  
...  
Keyword(s):  
Gene Expression ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Regulatory Elements ◽  
Genome Wide Association Studies ◽  
Expression Levels ◽  
Chromatin Loops ◽  
Coding Regions ◽  
Affect Gene Expression ◽  
Gene Expression Levels

Abstract Background Genome-wide association studies (GWASs) have identified single-nucleotide polymorphisms (SNPs) that may be genetic factors underlying Alzheimer’s disease (AD). However, how these AD-associated SNPs (AD SNPs) contribute to the pathogenesis of this disease is poorly understood because most of them are located in non-coding regions, such as introns and intergenic regions. Previous studies reported that some disease-associated SNPs affect regulatory elements including enhancers. We hypothesized that non-coding AD SNPs are located in enhancers and affect gene expression levels via chromatin loops. Methods To characterize AD SNPs within non-coding regions, we extracted 406 AD SNPs with GWAS p-values of less than 1.00 × 10− 6 from the GWAS catalog database. Of these, we selected 392 SNPs within non-coding regions. Next, we checked whether those non-coding AD SNPs were located in enhancers that typically regulate gene expression levels using publicly available data for enhancers that were predicted in 127 human tissues or cell types. We sought expression quantitative trait locus (eQTL) genes affected by non-coding AD SNPs within enhancers because enhancers are regulatory elements that influence the gene expression levels. To elucidate how the non-coding AD SNPs within enhancers affect the gene expression levels, we identified chromatin-chromatin interactions by Hi-C experiments. Results We report the following findings: (1) nearly 30% of non-coding AD SNPs are located in enhancers; (2) eQTL genes affected by non-coding AD SNPs within enhancers are associated with amyloid beta clearance, synaptic transmission, and immune responses; (3) 95% of the AD SNPs located in enhancers co-localize with their eQTL genes in topologically associating domains suggesting that regulation may occur through chromatin higher-order structures; (4) rs1476679 spatially contacts the promoters of eQTL genes via CTCF-CTCF interactions; (5) the effect of other AD SNPs such as rs7364180 is likely to be, at least in part, indirect through regulation of transcription factors that in turn regulate AD associated genes. Conclusion Our results suggest that non-coding AD SNPs may affect the function of enhancers thereby influencing the expression levels of surrounding or distant genes via chromatin loops. This result may explain how some non-coding AD SNPs contribute to AD pathogenesis.

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