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 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 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 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 Self-Reported Sleep Apnea and Dementia Risk: Findings from the Prevention of Alzheimer's Disease with Vitamin E and Selenium Trial

2016 ◽  
Vol 64 (12) ◽  
pp. 2472-2478 ◽  
Author(s):  
Xiuhua Ding ◽  
Richard J. Kryscio ◽  
Joshua Turner ◽  
Gregory A. Jicha ◽  
Gregory Cooper ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Vitamin E ◽  
Sleep Apnea ◽  
Dementia Risk

scholarly journals The frequency and influence of dementia risk factors in prodromal Alzheimer's disease

2017 ◽  
Vol 56 ◽  
pp. 33-40 ◽  
Author(s):  
Isabelle Bos ◽  
Stephanie J. Vos ◽  
Lutz Frölich ◽  
Johannes Kornhuber ◽  
Jens Wiltfang ◽  
...  
Keyword(s):  
Risk Factors ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Dementia Risk ◽  
Prodromal Alzheimer’S Disease

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 Genome research in pre-dementia stages of Alzheimer's disease

2016 ◽  
Vol 18 ◽  
Author(s):  
Sonia Moreno-Grau ◽  
Agustín Ruiz
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Late Onset ◽  
Subjective Cognitive Decline ◽  
Genetic Profile ◽  
Amyloid Deposits ◽  
Dementia Risk ◽  
Meta Analyses ◽  
Brain Insults

Genetic characterization of individuals at risk of Alzheimer's disease (AD), i.e. people having amyloid deposits in the brain without symptoms, people suffering from subjective cognitive decline (SCD) or mild cognitive impairment (MCI), has spurred the interests of researchers. However, their pre-dementia genetic profile remains mostly unexplored. In this study, we reviewed the loci related to phenotypes of AD, MCI and SCD from literature and performed the first meta-analyses evaluating the role of apolipoprotein E (APOE) in the risk of conversion from a healthy status to MCI and SCD. For AD dementia risk, an increased number of loci have been identified; to date, 28 genes have been associated with Late Onset AD. In MCI syndrome,APOEis confirmed as a pheno-conversion factor leading from MCI to AD, and clusterin is a promising candidate. Additionally, our meta-analyses revealedAPOEas genetic risk factor to convert from a healthy status to MCI [OR = 1.849 (1.587–2.153);P = 2.80  × 10−15] and to a lesser extent from healthy status to SCD [OR = 1.151 (1.015–1.304);P = 0.028]. Thus, we believe that genetic studies in longitudinal SCD and MCI series may provide new therapeutic targets and improve the existing knowledge of AD. This type of studies must be completed on healthy subjects to better understand the natural disease resistance to brain insults and neurodegeneration.

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