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

Cdc42GAP deficiency contributes to the Alzheimer's disease phenotype.

Brain : a journal of neurology - 3 Oct 2023

Zhu Mengjuan, Xiao Bin, Xue Tao, Qin Sifei, Ding Jiuyang, Wu Yue, Tang Qingqiu, Huang Mengfan, Zhao Na, Ye Yingshan, Zhang Yuning, Zhang Boya, Li Juan, Guo Fukun, Jiang Yong, Zhang Lin, Zhang Lu

Abstract excerpt

Alzheimer's disease, the most common cause of dementia, is a chronic degenerative disease with typical pathological features of extracellular senile plaques and intracellular neurofibrillary tangles and a significant decrease in the density of neuronal dendritic spines. Cdc42 is a member of the small G protein family that plays an important role in regulating synaptic plasticity and is regulated by Cdc42GAP,...

Read the complete abstract on PubMed

Topics

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

Share to Actins
Share to Alzheimer Disease

Methodology Data sources Editorial policy Privacy Delete account & data About Contact Helena Bioinformatics

Share to Glycogen Synthase Kinase 3 beta

Share to GTPase-Activating Proteins

Share to Neurons

Share to Phosphorylation

Share to tau Proteins

Source

Identifiers

PMID: 37254741
DOI: 10.1093/brain/awad184

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-08.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Cdc42GAP deficiency contributes to the Alzheimer's disease phenotype.PMID 37254741Read ↗

Loss of amyloid precursor protein in a mouse model of Niemann-Pick type C disease exacerbates its phenotype and disrupts tau homeostasis.Semantic proximity Read ↗

Nodes and biological processes identified on the basis of network analysis in the brain of the senescence accelerated mice as an Alzheimer's disease animal modelSemantic proximity Read ↗

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

CD2AP deficiency aggravates Alzheimer's disease phenotypes and pathology through p38 MAPK activation.Semantic proximity Read ↗

Mutant human APP exacerbates pathology in a mouse model of NPC and its reversal by a β-cyclodextrin.Semantic proximity Read ↗

RAPGEF2 mediates oligomeric Aβ-induced synaptic loss and cognitive dysfunction in Alzheimer’s diseaseSemantic proximity Read ↗

EPAC2 knockout causes abnormal tau pathology through calpain-mediated CDK5 activationSemantic proximity Read ↗

Identification of the Role of miR-142-5p in Alzheimer’s Disease by Comparative Bioinformatics and Cellular AnalysisSemantic proximity Read ↗

Deletion of Gadd45a Expression in Mice Leads to Cognitive and Synaptic Impairment Associated with Alzheimer’s Disease HallmarksSemantic proximity Read ↗

mTOR in Down syndrome: Role in Aß and tau neuropathology and transition to Alzheimer disease-like dementiaSemantic proximity Read ↗

Cdc42 GTPase-activating protein deficiency promotes genomic instability and premature aging-like phenotypes.Semantic proximity Read ↗

cindr, the Drosophila Homolog of the CD2AP Alzheimer’s Disease Risk Gene, Is Required for Synaptic Transmission and ProteostasisSemantic proximity Read ↗

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