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

Alternative splicing of exon 10 in the tau gene as a target for treatment of tauopathies.

BMC neuroscience - 3 Dec 2008

Zhou Jianhua, Yu Qingming, Zou Tie

Abstract excerpt

Tau aggregation is one of the major features in Alzheimer's disease and in several other tauopathies, including frontotemporal dementia with Parkinsonism linked to chromosome 17 (FTDP-17), and progressive supranuclear palsy (PSP). More than 35 mutations in the tau gene have been identified from FTDP-17 patients. A group of these mutations alters splicing of exon 10, resulting in an increase in exon 10 inclusion...

Read the complete abstract on PubMed

Topics

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

Share to Alternative Splicing
Share to Alzheimer Disease
Share to Alzheimer's disease research and treatments

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Dementia

Share to Mutation

Share to tau Proteins

Share to Tauopathies

Source

Open in PubMed Open full text

Identifiers

PMID: 19090983
DOI: 10.1186/1471-2202-9-S2-S10
PMCID: PMC2604894

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 2 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Alternative splicing of exon 10 in the tau gene as a target for treatment of tauopathies.PMID 19090983Read ↗

The Tau N279K Exon 10 Splicing Mutation Recapitulates Frontotemporal Dementia and Parkinsonism Linked to Chromosome 17 Tauopathy in a Mouse ModelSemantic proximity Read ↗

5' splice site mutations in tau associated with the inherited dementia FTDP-17 affect a stem-loop structure that regulates alternative splicing of exon 10.Semantic proximity Read ↗

Tau exon 10 alternative splicing and tauopathiesSemantic proximity Read ↗

FTDP‐17 mutations N279K and S305N in tau produce increased splicing of exon 10Semantic proximity Read ↗

Correction of alternative splicing of tau in frontotemporal dementia and parkinsonism linked to chromosome 17.Semantic proximity Read ↗

Aberrant splicing of tau pre-mRNA caused by intronic mutations associated with the inherited dementia frontotemporal dementia with parkinsonism linked to chromosome 17.Semantic proximity Read ↗

Tau exon 10, whose missplicing causes frontotemporal dementia, is regulated by an intricate interplay of cis elements and trans factors.Semantic proximity Read ↗

Missense and silent tau gene mutations cause frontotemporal dementia with parkinsonism-chromosome 17 type, by affecting multiple alternative RNA splicing regulatory elements.Semantic proximity Read ↗

HCS-Splice: A High-Content Screening Method to Advance the Discovery of RNA Splicing-Modulating Therapeutics.Semantic proximity Read ↗

HCS-Splice: A High-Content Screening Method to Advance the Discovery of RNA Splicing-Modulating TherapeuticsSemantic proximity Read ↗

<i>MAPT</i> Splicing Modulators as a Therapeutic Strategy for TauopathiesSemantic proximity Read ↗

MAPT splicing modulators reduce 4R tau and rescue tauopathy phenotypes in human neurons and in a mouse model.Semantic proximity Read ↗

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