Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Protein restriction slows the development and progression of Alzheimer's disease in mice

ABSTRACT: Targeted lipidomics of 3xTg and non-transgenic mouse brain on protein restricted diet

INSTRUMENT(S): 6495C Triple Quadrupole LC/MS

ORGANISM(S): Mus Musculus (ncbitaxon:10090)

SUBMITTER: Judith Simcox

PROVIDER: MSV000094815 | MassIVE | Tue May 21 08:16:00 BST 2024

REPOSITORIES: MassIVE

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Protein restriction slows the development and progression of Alzheimer's disease in mice

Project description:Untargeted lipidomics of 3xTg and non-transgenic mouse brain on protein restricted diet

2024-05-21 | MSV000094819 | MassIVE

Protein restriction slows the development and progression of Alzheimer's disease in mice

Project description:Targeted metabolomics of 3xTg and non-transgenic mouse brain on protein restricted diet

2024-05-21 | MSV000094816 | MassIVE

Calorie restriction slows age-related microbiota changes in an Alzheimer's disease model in female mice.

Project description:Alzheimer's disease (AD) affects an estimated 5.8 million Americans, and advanced age is the greatest risk factor. AD patients have altered intestinal microbiota. Accordingly, depleting intestinal microbiota in AD animal models reduces amyloid-beta (A?) plaque deposition. Age-related changes in the microbiota contribute to immunologic and physiologic decline. Translationally relevant dietary manipulations may be an effective approach to slow microbiota changes during aging. We previously showed that calorie restriction (CR) reduced brain A? deposition in the well-established Tg2576 mouse model of AD. Presently, we investigated whether CR alters the microbiome during aging. We found that female Tg2576 mice have more substantial age-related microbiome changes compared to wildtype (WT) mice, including an increase in Bacteroides, which were normalized by CR. Specific gut microbiota changes were linked to A? levels, with greater effects in females than in males. In the gut, Tg2576 female mice had an enhanced intestinal inflammatory transcriptional profile, which was reversed by CR. Furthermore, we demonstrate that Bacteroides colonization exacerbates A? deposition, which may be a mechanism whereby the gut impacts AD pathogenesis. These results suggest that long-term CR may alter the gut environment and prevent the expansion of microbes that contribute to age-related cognitive decline.

| S-EPMC6884494 | biostudies-literature

Protein restriction slows the progression of Alzheimer's disease in a mouse model

Project description:plasma metabolomics done after restriction of dietary protein in AD mice.

2024-06-11 | MSV000094992 | MassIVE

IKKβ slows Huntington's disease progression in R6/1 mice.

Project description:Neuroinflammation is an important contributor to neuronal pathology and death in neurodegenerative diseases and neuronal injury. Therapeutic interventions blocking the activity of the inflammatory kinase IKKβ, a key regulator of neuroinflammatory pathways, is protective in several animal models of neurodegenerative disease and neuronal injury. In Huntington's disease (HD), however, significant questions exist as to the impact of blocking or diminishing the activity of IKKβ on HD pathology given its potential role in Huntingtin (HTT) degradation. In cell culture, IKKβ phosphorylates HTT serine (S) 13 and activates HTT degradation, a process that becomes impaired with polyQ expansion. To investigate the in vivo relationship of IKKβ to HTT S13 phosphorylation and HD progression, we crossed conditional tamoxifen-inducible IKKβ knockout mice with R6/1 HD mice. Behavioral assays in these mice showed a significant worsening of HD pathological phenotypes. The increased behavioral pathology correlated with reduced levels of endogenous mouse full-length phospho-S13 HTT, supporting the importance of IKKβ in the phosphorylation of HTT S13 in vivo. Notably, many striatal autophagy genes were up-regulated in HD vs. control mice; however, IKKβ knockout partially reduced this up-regulation in HD, increased striatal neurodegeneration, and enhanced an activated microglial response. We propose that IKKβ is protective in striatal neurons early in HD progression via phosphorylation of HTT S13. As IKKβ is also required for up-regulation of some autophagy genes and HTT is a scaffold for selective autophagy, IKKβ may influence autophagy through multiple mechanisms to maintain healthy striatal function, thereby reducing neuronal degeneration to slow HD onset.

| S-EPMC6561205 | biostudies-literature

Nuclear tRNA sequestering slows aging by a mechanism similar to dietary restriction

Project description:Dietary restriction (DR) is the best-characterized intervention for slowing aging, and reduced signaling through the target of rapamycin (TOR) kinase is believed to be one of the key mechanisms by which DR extends life span in organisms from yeast to mammals. Here we describe a role for nuclear sequestration of tRNA in yeast replicative life span (RLS) extension from DR. DR causes the nuclear tRNA exporter Los1 to become depleted from the nucleus by a mechanism that requires the DNA damage response factor Rad53, and deletion of LOS1 or overexpression of RAD53 is sufficient to extend RLS. We further report that activation of the nitrogen responsive transcription factor Gln3 is the primary mechanism by which DR extends RLS. Gln3 is activated by both branches of the DR response and is required for life span extension. Overexpression of Gln3 extends RLS by approximately 50%. In order to identify potential factors acting to modulate longevity downstream of Los1, we used microarray analysis to compare the gene expression profiles of wild type and LOS1 knockout cells under non-restricted conditions cultured overnight prior to RNA isolation.

2015-02-03 | E-GEOD-37241 | biostudies-arrayexpress

GNPS - Protein restriction slows the progression of Alzheimer's disease in a mouse model

Project description:plasma metabolomics done after restriction of dietary protein in AD mice.

2024-06-11 | MSV000094992 | GNPS

Calorie/Dietary Restriction and Resveratrol in Female Drosophila Melanogaster Head/Thorax

Project description:Feeding resveratrol to Drosophila melanogaster extends lifespan. Studies of microarray show similarities between calorie/dietary restriction and resveratrol on both a gene expression and biological pathway level. 9 samples: 3 biological replicates each of normal diet, restricted diet and normal diet plus resveratrol

2011-07-20 | E-GEOD-26724 | biostudies-arrayexpress

An intermittent caloric restriction / medium fat diet protects liver from the progression of non-alcoholic fatty liver disease in C57BL/6J mice

Project description:Background & Aims: In this study, we investigated metabolic and molecular effects of weekly intervening 30% calorie restriction on long term natural progression of non-alcoholic fatty liver disease (NAFLD), which was induced by a medium fat diet. Methods: Male C57BL/6J mice of 9 weeks old received either (1) a control (C), (2) a calorie restricted (CR), (3) a medium fat (MF; 25%fat) or (4) an intermittent diet (ID), a weekly alternating diet consisting of calorie restriction and medium fat diet ad libitum until sacrifice at the age of 12 months. Various metabolic and molecular features of the liver were examined. Results: The ID regimen improved the status of a range of metabolic parameters and showed no progression to NAFLD: proper glucose tolerance, low hepatic triglyceride content, low plasma alanine aminotransferase and no abnormalities in its liver morphological features; similarly to that of CR. In contrast, the metabolic parameters in a number of the C and MF animals indicated development of NAFLD and hepatic fibrosis, which was positively correlated with body weight. Despite the metabolic phenotypes similarity, the liver gene expression profile of ID-fed mice did not reflect that of CR mice and resembled more to C and MF-fed mice with similar low body weight. Conclusions: Our study reveals that ID is beneficial for metabolic health and prevents the development of NAFLD in mice, with a gene expression profile similar to C and MF diet in a body weight-dependent manner.

2018-05-09 | GSE53188 | GEO

Deficiency in Sirtuin3 rewires mitochondrial metabolism and increases maximum lifespan under caloric restriction - Mitochondrial Acetylation Stoichiometry

Project description:Quantification of acetylation stoichiometry from mitochondrial enriched proteins from mouse livers. Conditions compared include genotype, diet, and age; i.e. Sirt3 KO vs Sirt3 WT, caloric restricted (CR) diet vs control diet (CD), and 5 months old vs 25 months old.

2021-03-23 | MSV000087085 | MassIVE

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data