Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

FAD4T mouse model reflects Alzheimer’s disease pathobiology in bone marrow-brain axis

ABSTRACT: In this study, we established a FAD4T mouse model, which reflects Alzheimer’s disease pathobiology in bone marrow-brain axis.

ORGANISM(S): Mus musculus

PROVIDER: GSE214917 | GEO | 2025/07/23

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

FAD4T mouse model reflects Alzheimer’s disease pathobiology in bone marrow-brain axis

Project description:FAD4T mouse model reflects Alzheimer’s disease pathobiology in bone marrow-brain axis

| PRJNA887736 | ENA

The brain-bone marrow axis and its implications for chronic traumatic brain injury.

Project description:Traumatic brain injury (TBI) causes acute and chronic alterations in systemic immune function which contribute to posttraumatic neuroinflammation and neurodegeneration. However, how TBI affects bone marrow (BM) hematopoietic stem/progenitor cells chronically and to what extent such changes may negatively impact innate immunity and neurological function has not been examined. To further understand the role of BM cell derivatives on TBI outcome, we generated BM chimeric mice by transplanting BM from chronically injured or sham congenic donor mice into otherwise healthy, age-matched, irradiated hosts. After 8 weeks of reconstitution, peripheral myeloid cells from TBI→WT mice showed significantly higher oxidative stress levels and reduced phagocytic activity. At eight months after reconstitution, TBI→WT chimeric mice were leukopenic, with continued alterations in phagocytosis and oxidative stress responses, as well as persistent neurological deficits. Gene expression analysis revealed BM-driven changes in neuroinflammation and neuropathology after 8 weeks and 8 months of reconstitution, respectively. Chimeric mice subjected to TBI showed that longer reconstitution periods were associated with increased microgliosis and leukocyte infiltration. Thus, TBI causes chronic activation and progressive dysfunction of the BM stem/progenitor cell pool, which drives long-term deficits in innate immunity and neurological function, as well as altered sensitivity to subsequent brain injury.

| S-EPMC10543403 | biostudies-literature

Brain-Gut-Bone Marrow Axis: Implications for Hypertension and Related Therapeutics.

Project description:Hypertension is the most prevalent modifiable risk factor for cardiovascular disease and disorders directly influencing cardiovascular disease morbidity and mortality, such as diabetes mellitus, chronic kidney disease, obstructive sleep apnea, etc. Despite aggressive attempts to influence lifestyle modifications and advances in pharmacotherapeutics, a large percentage of patients still do not achieve recommended blood pressure control worldwide. Thus, we think that mechanism-based novel strategies should be considered to significantly improve control and management of hypertension. The overall objective of this review is to summarize implications of peripheral- and neuroinflammation as well as the autonomic nervous system-bone marrow communication in hematopoietic cell homeostasis and their impact on hypertension pathophysiology. In addition, we discuss the novel and emerging field of intestinal microbiota and roles of gut permeability and dysbiosis in cardiovascular disease and hypertension. Finally, we propose a brain-gut-bone marrow triangular interaction hypothesis and discuss its potential in the development of novel therapies for hypertension.

| S-EPMC4834860 | biostudies-literature

Understanding Early Stage Myelodysplastic Syndrome Pathobiology

Project description:Understanding Early Stage Myelodysplastic Syndrome Pathobiology

| PRJNA476461 | ENA

Unwavering Pathobiology of Volumetric Muscle Loss Injury

Project description:Unwavering Pathobiology of Volumetric Muscle Loss Injury

| PRJNA472640 | ENA

Genetics and Pathobiology of Cutaneous Mosaic Disorders

Project description:Genetics and Pathobiology of Cutaneous Mosaic Disorders

| PRJNA1160915 | ENA

Genetics and Pathobiology of Cutaneous Mosaic Disorders

Project description:Genetics and Pathobiology of Cutaneous Mosaic Disorders

| PRJNA1160916 | ENA

Genetics and Pathobiology of Disorders of Keratinization

Project description:Genetics and Pathobiology of Disorders of Keratinization

| PRJNA1291281 | ENA

Genetics and Pathobiology of Disorders of Keratinization

Project description:Genetics and Pathobiology of Disorders of Keratinization

| PRJNA1291282 | ENA

Methionine restriction alleviate cognitive dysfunction in Alzheimer’s disease: the mediating roles of gut microbiota-brain axis

Project description:We reported that a 4-month methionine-restricted diet (MR) intervention reduced the cognitive impairment in Alzheimer’s disease. Here, we introduce the transcriptomics data of the mouse hippocampus to further study how MR regulates important biological processes and pathways. After mapping clean RNA-seq reads of all mice against the Mus musculus genome, we detected 56,412 genes (including 12,527 new predicted genes) with fragments per kilobase of transcripts per million mapped reads (FPKM) value. Gene set enrichment analysis (GSEA) was used for pathway or functional analysis of RNA-seq data.

2021-12-31 | GSE164618 | GEO

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