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

AAV-GRN partially corrects motor deficits and ALS/FTLD-related pathology in Tmem106bGrn mice

28 Jun 2023

Abstract excerpt

Loss of function of progranulin (PGRN), encoded by the granulin ( GRN ) gene, is implicated in several neurodegenerative diseases. Several therapeutics to boost PGRN levels are currently in clinical trials. However, it is difficult to test the efficacy of PGRN-enhancing drugs in mouse models due to the mild phenotypes of Grn −/− mice. Recently, mice deficient in both PGRN and TMEM106B were shown to develop severe...

Read the complete abstract on PubMed

Topics

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

Share to Amyotrophic Lateral Sclerosis Research
Share to Neurogenetic and Muscular Disorders Research
Share to Parkinson's Disease Mechanisms and Treatments

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Source

Identifiers

PMID: 37519899
DOI: 10.1016/j.isci.2023.107247

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

AAV-GRN partially corrects motor deficits and ALS/FTLD-related pathology in Tmem106bGrn micePMID 37519899Read ↗

Loss of Tmem106b exacerbates FTLD pathologies and causes motor deficits in progranulin-deficient mice.Semantic proximity Read ↗

Loss of Tmem106b is unable to ameliorate frontotemporal dementia-like phenotypes in an AAV mouse model of C9ORF72-repeat induced toxicitySemantic proximity Read ↗

PGRN deficiency exacerbates, whereas a brain penetrant PGRN derivative protects, GBA1 mutation-associated pathologies and diseases.Semantic proximity Read ↗

Loss of TMEM106B Ameliorates Lysosomal and Frontotemporal Dementia-Related Phenotypes in Progranulin-Deficient Mice.Semantic proximity Read ↗

Human progranulin-expressing mice as a novel tool for the development of progranulin-modulating therapeuticsSemantic proximity Read ↗

Loss of TMEM106B and PGRN leads to severe lysosomal abnormalities and neurodegeneration in miceSemantic proximity Read ↗

Progranulin: a new avenue towards the understanding and treatment of neurodegenerative disease.Semantic proximity Read ↗

Rescue of FTLD-associated TDP-43 pathology and neurodegeneration by peripheral AAV-mediated expression of brain-penetrant progranulinSemantic proximity Read ↗

Adeno-associated virus serotype 1-based gene therapy for FTD caused by GRN mutations.Semantic proximity Read ↗

Mechanisms of Granulin Deficiency: Lessons from Cellular and Animal ModelsSemantic proximity Read ↗

Granulin loss and TMEM106B risk converge on lysosomal C-terminal fragment pathology in frontotemporal dementiaSemantic proximity Read ↗

AAV-mediated progranulin delivery to a mouse model of progranulin deficiency causes T cell-mediated hippocampal degenerationSemantic proximity Read ↗

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