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

Targeting histone K4 trimethylation for treatment of cognitive and synaptic deficits in mouse models of Alzheimer’s disease

9 Dec 2020

Abstract excerpt

, which encodes serum and glucocorticoid-regulated kinase 1, is also significantly elevated in PFC of patients with AD. Administration of a specific Sgk1 inhibitor reduces hyperphosphorylated tau protein, restores PFC glutamatergic synaptic function, and ameliorates memory deficits in AD mice. These results have found a novel epigenetic mechanism and a potential therapeutic strategy for AD and related...

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 Epigenetics and DNA Methylation
Share to Nuclear Receptors and Signaling

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Source

Identifiers

PMID: 33298440
DOI: 10.1126/sciadv.abc8096

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 6 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Targeting histone K4 trimethylation for treatment of cognitive and synaptic deficits in mouse models of Alzheimer’s diseasePMID 33298440Read ↗

Restoring the epigenome in Alzheimer's disease: advancing HDAC inhibitors as therapeutic agentsSemantic proximity Read ↗

Inhibition of histone methyltransferase Smyd3 rescues NMDAR and cognitive deficits in a tauopathy mouse modelSemantic proximity Read ↗

Histone H3 Lysine 4 and 27 Trimethylation Landscape of Human Alzheimer’s DiseaseSemantic proximity Read ↗

Inhibition of EHMT1/2 rescues synaptic and cognitive functions for Alzheimer’s diseaseSemantic proximity Read ↗

Neuronal HDAC9: A key regulator of cognitive and synaptic aging, rescuing Alzheimer’s disease-related phenotypesSemantic proximity Read ↗

Targeting histone-modifications in Alzheimer's disease. What is the evidence that this is a promising therapeutic avenue?Semantic proximity Read ↗

Dysregulation of histone acetylation pathways in hippocampus and frontal cortex of Alzheimer's disease patientsSemantic proximity Read ↗

Histone Deacetylase Inhibition in Alzheimer’s Disease: Molecular Mechanisms, Therapeutic Potential, and Future PerspectivesSemantic proximity Read ↗

HDAC3 as an Emerging Therapeutic Target for Alzheimer's Disease and other Neurological DisordersSemantic proximity Read ↗

Neuronal HDAC9: A key regulator of cognitive and synaptic aging, rescuing Alzheimer's disease-related phenotypes.Semantic proximity Read ↗

The role of histone acetylation in age-associated memory impairment and Alzheimer’s diseaseSemantic proximity Read ↗

Histone acetylation in neuronal (dys)function.Semantic proximity Read ↗

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