Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

p38α‐MAPK‐deficient myeloid cells ameliorate symptoms and pathology of APP ‐transgenic Alzheimer's disease mice

31 Jul 2022

Abstract excerpt

Alzheimer's disease (AD), the most common cause of dementia in the elderly, is pathologically characterized by extracellular deposition of amyloid-β peptides (Aβ) and microglia-dominated inflammatory activation in the brain. p38α-MAPK is activated in both neurons and microglia. How p38α-MAPK in microglia contributes to AD pathogenesis remains unclear. In this study, we conditionally knocked out p38α-MAPK in all...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Alzheimer's disease research and treatments
Share to Immune cells in cancer
Share to Neuroinflammation and Neurodegeneration Mechanisms

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Source

Identifiers

PMID: 35909315
DOI: 10.1111/acel.13679

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 3 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

p38α‐MAPK‐deficient myeloid cells ameliorate symptoms and pathology of APP ‐transgenic Alzheimer's disease micePMID 35909315Read ↗

Neuronal deficiency of p38α‐MAPK ameliorates symptoms and pathology of APP or Tau‐transgenic Alzheimer’s mouse modelsSemantic proximity Read ↗

Microglia in Alzheimer’s DiseaseSemantic proximity Read ↗

The dual role of microglia in Alzheimer’s disease: from immune regulation to pathological progressionSemantic proximity Read ↗

Microglial ERK signaling is a critical regulator of pro-inflammatory immune responses in Alzheimer’s diseaseSemantic proximity Read ↗

The Functions and Phenotypes of Microglia in Alzheimer's Disease.Semantic proximity Read ↗

Microglia-Associated Neuroinflammation in Alzheimer’s DiseaseSemantic proximity Read ↗

Fibrillar Aβ triggers microglial proteome alterations and dysfunction in Alzheimer mouse modelsSemantic proximity Read ↗

Distinct inflammatory phenotypes of microglia and monocyte-derived macrophages in Alzheimer's disease models: effects of aging and amyloid pathology.Semantic proximity Read ↗

Transplantation of wild-type hematopoietic stem and progenitor cells rescue Alzheimer’s disease in a mouse model and highlights the central role of microglia in disease pathogenesisSemantic proximity Read ↗

Fibrillar Aβ triggers microglial proteome alterations and dysfunction in Alzheimer mouse modelsSemantic proximity Read ↗

Conditional Genetic Deletion of CSF1 Receptor in Microglia Ameliorates the Physiopathology of Alzheimer’s DiseaseSemantic proximity Read ↗

An overview on microglial origin, distribution, and phenotype in Alzheimer's disease.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.