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

Increased expression of the frontotemporal dementia risk factor TMEM106B causes C9orf72-dependent alterations in lysosomes.

Human molecular genetics - 1 Jul 2016

Busch Johanna I, Unger Travis L, Jain Nimansha, Tyler Skrinak R, Charan Rakshita A, Chen-Plotkin Alice S

Abstract excerpt

Frontotemporal lobar degeneration with TDP-43 inclusions (FTLD-TDP) is an important cause of dementia in individuals under age 65. Common variants in the TMEM106B gene were previously discovered by genome-wide association to confer genetic risk for FTLD-TDP (p = 1 × 10-11, OR = 1.6). Furthermore, TMEM106B may act as a genetic modifier affecting age at onset and age at death in the Mendelian subgoup of FTLD-TDP...

Read the complete abstract on PubMed

Topics

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

Share to C9orf72 Protein
Share to Cell Culture Techniques

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Frontotemporal Dementia

Share to Frontotemporal Lobar Degeneration

Share to Genes, Regulator

Share to Inclusion Bodies

Share to Lysosomes

Share to Primary Cell Culture

Source

Open in PubMed Open full text

Identifiers

PMID: 27126638
DOI: 10.1093/hmg/ddw127
PMCID: PMC5181637

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

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

Increased expression of the frontotemporal dementia risk factor TMEM106B causes C9orf72-dependent alterations in lysosomes.PMID 27126638Read ↗

What we know about TMEM106B in neurodegeneration.Semantic proximity Read ↗

The frontotemporal lobar degeneration risk factor, TMEM106B, regulates lysosomal morphology and functionSemantic proximity Read ↗

TMEM106B, a frontotemporal lobar dementia (FTLD) modifier, associates with FTD-3-linked CHMP2B, a complex of ESCRT-III.Semantic proximity Read ↗

Loss of TMEM106B exacerbates C9ALS/FTD DPR pathology by disrupting autophagosome maturationSemantic proximity Read ↗

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

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

Loss of TMEM106B leads to myelination deficits: implications for frontotemporal dementia treatment strategies.Semantic proximity Read ↗

Expression of TMEM106B, the frontotemporal lobar degeneration-associated protein, in normal and diseased human brain.Semantic proximity Read ↗

The FTLD Risk Factor TMEM106B Regulates the Transport of Lysosomes at the Axon Initial Segment of Motoneurons.Semantic proximity Read ↗

TMEM106B a novel risk factor for frontotemporal lobar degeneration.Semantic proximity Read ↗

TMEM106B expression is reduced in Alzheimer’s disease brainsSemantic proximity Read ↗

Membrane orientation and subcellular localization of transmembrane protein 106B (TMEM106B), a major risk factor for frontotemporal lobar degeneration.Semantic proximity Read ↗

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