Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Immune Receptor Lag3 Deletion Alleviates Neurodegeneration Phenotypes in a Mouse Model of Alzheimer’s Disease

ABSTRACT: Immune Receptor Lag3 Deletion Alleviates Neurodegeneration Phenotypes in a Mouse Model of Alzheimer’s Disease

PROVIDER: PRJNA1314557 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Similar Datasets

Immune Receptor Lag3 Deletion Alleviates Neurodegeneration Phenotypes in a Mouse Model of Alzheimer’s Disease

Project description:Alzheimer’s disease (AD) is the leading cause of dementia, but effective treatments remail unavailable. Using the 5xFAD familial AD mouse model, we show that deletion of the immune checkpoint receptor Lymphocyte activation gene 3 (Lag3) reduces amyloidosis, microgliosis, and neurodegeneration-related behavioral deficits. Transcriptional profiling revealed that Lag3 deletion reverses aberrant expression of disease-associated microglia (DAM) genes and decreased CD8+ T cells infiltration in the brain. These findings suggest that Lag3 regulates microglia function and may represent a potential therapeutic target for AD.

2025-09-10 | GSE307127 | GEO

Z-RNA drives Tau-mediated neurodegeneration of Alzheimer’s disease [RNA-Seq]

Project description:Tau aggregates lead to progressive neurodegeneration in Alzheimer’s disease (AD) (ref). Neuron death is one of the hallmarks of neurodegeneration (ref). However, the pathological influence of neuronal death is undetermined, and the connection between Tau aggregates and neuronal death remains elusive. Here we demonstrated the essential role of neuron death in Tau-related neurodegeneration. Tau-neurons died in necroptosis, dependent on ZBP1 sensitized by Z-RNAs (an unusual left-handed conformation). Those endogenous Z-RNAs were transcripts of reactivated transposable elements (TEs) originally silenced in heterochromatin.

2023-11-22 | GSE248067 | GEO

Z-RNA drives Tau-mediated neurodegeneration of Alzheimer’s disease [lncRNA-Seq]

2023-11-22 | GSE248068 | GEO

Z-RNA drives Tau-mediated neurodegeneration of Alzheimer’s disease

Project description:Z-RNA drives Tau-mediated neurodegeneration of Alzheimer’s disease

| PRJNA1041713 | ENA

Z-RNA drives Tau-mediated neurodegeneration of Alzheimer’s disease [RIP-Seq]

Project description:Tau aggregates lead to progressive neurodegeneration in Alzheimer’s disease (AD). Neuron death is one of the hallmarks of neurodegeneration.However, the pathological influence of neuronal death is undetermined, and the connection between Tau aggregates and neuronal death remains elusive. Here we demonstrated the essential role of neuron death in Tau-related neurodegeneration. Tau-neurons died in necroptosis, dependent on ZBP1 sensitized by Z-RNAs (an unusual left-handed conformation). Those endogenous Z-RNAs were transcripts of reactivated transposable elements (TEs) originally silenced in heterochromatin.

2023-11-22 | GSE248069 | GEO

Transcription profiling of mouse CD4+ CD25+, CD4+ CD25- CD45RBlow LAG3+ and CD4+ CD25- CD45RBlow LAG3- T cells

Project description:Comparison of gene expression profile of CD4+ CD25+, CD4+ CD25- CD45RBlow LAG3+ and CD4+ CD25- CD45RBlow LAG3- T cells. Naive CD4+CD25-CD45RBhigh T cells were used as a reference for pair comparison with values from the three other subsets.

2009-08-19 | E-MEXP-1343 | biostudies-arrayexpress

Gamma entrainment binds higher order brain regions and alleviates neurodegeneration

Project description:Gamma entrainment binds higher order brain regions and alleviates neurodegeneration

| PRJNA474231 | ENA

Temporal tracking of microglia activation in neurodegeneration at single-cell resolution

Project description:In this study, we used single-cell RNA-sequencing to gain unprecedented insight into the phenotypic heterogeneity and the transcriptional dynamics of microglia cells during the progression of neurodegeneration. Briefly, by using a severe neurodegeneration mouse model with Alzheimer’s-like pathology and phenotypes (CK-p25 model), we surveyed microglia activation by RNA sequencing longitudinally at fine temporal- and single-cell resolution. In summary, our work identified previously unobserved heterogeneity in the response of microglia to neurodegeneration, discovered novel microglia cell states, revealed the trajectory of cellular reprogramming of microglia in response to neurodegeneration, and uncovered the underlying transcriptional programs. These insights into the molecular programs underlying microglia activation provided by our study may pave the way for designing new rational and efficient strategies to treat Alzheimer’s and other neurodegenerative diseases.

2017-10-10 | GSE103334 | GEO

Non-Mutated Human Tau Stimulates Alzheimer’s Disease-Relevant Neurodegeneration in a Microglia-Dependent Manner

Project description:The accumulation of abnormal, non-mutated tau protein is a key pathological hallmark of Alzheimer’s disease (AD). Despite its strong association with disease progression, the mechanisms by which tau drives neurodegeneration in the intact brain remain poorly understood. Here, we selectively expressed non-mutated or mutated MAPT in neurons across the brain and observed neurodegeneration in the hippocampus, especially associated with non-mutated human tau. Single-nuclei RNA sequencing confirmed a selective loss of hippocampal excitatory neurons and revealed the upregulation of neurodegeneration-related pathways in the affected populations. The accumulation of phosphorylated tau was accompanied by cellular stress in neurons and reactive gliosis in multiple brain regions. Notably, the lifelong absence of microglia significantly and differentially influenced the extent of neurodegeneration in the hippocampus and thalamus. Therefore, our study established an AD-relevant tauopathy mouse model, elucidated both neuron-intrinsic and neuron-extrinsic responses, and highlighted a critical role for microglia in modulating tau-driven neurodegeneration.

2025-08-06 | GSE285945 | GEO

Microglia-specific loss of PU.1 function rescues neurodegenerative phenotypes in a mouse model of Alzheimer’s disease

Project description:Alzheimer’s disease (AD) is an age-related neurodegenerative disorder characterized by progressive decline of cognitive ability. An important component of AD, and other chronic neurodegenerative diseases, is generation of an innate inflammatory response within the CNS, characterized by activation of microglia, the resident immune cells of the brain. Transcription factor PU.1 has been known to play an important role in myeloid and lymphoid cell development, however its function in microglia and how it contributes to disease pathology is not well understood. Using transcriptional and chromatin state profiles during AD-like pathology in the CK-p25 mouse model of neurodegeneration, we showed that PU.1 specifically targets noncoding regions which regulate expression changes of immune response genes during AD, suggesting it may act as master regulator of microglia activation. Here, we examine the role of PU.1 in neurodegeneration by using a conditional knockout (cKO) cassette (Cx3cr1CreER+/-) to inducibly deplete PU.1 from microglia in the CK-p25 mouse model of neurodegeneration. We found that knocking out PU.1 rescues multiple neurodegenerative phenotypes. Specifically, PU.1 inhibition reduces neurodegeneration-specific increase in microglia cell number, improves neuronal survival and reverses functional synaptic plasticity deficits in the hippocampus of the CK-p25 mouse.

2021-01-01 | GSE117868 | 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