Article

Connecting HTT intermediate alleles and microRNA dysregulation to enhanced tauopathy in Late-Onset Alzheimer's Disease

2025-10-10

Abstract excerpt

<title>Abstract</title> Background Late-onset Alzheimer´s disease (LOAD) is a heterogenous disorder influenced by genetic factors. In fact, we have previously described intermediate alleles ( <italic>IAs</italic> ) in the huntingtin ( <italic>HTT</italic> ) gene as potential modifiers in around 6% of AD population. The caudate nucleus, the most affected region in Huntington's disease, is highly sensitive...

Topics

Open a Topic to create a Post that cites this publication.

Identifiers and source

Literature Corpus work: d444890f-258e-5e3f-9b3c-ce80a17e88cf
DOI: 10.21203/rs.3.rs-7621820/v1

Open publication

Related research

Semantic proximity does not establish scientific evidence.

Click a neighbor to travelStep 1 · 12 closest

Connecting HTT intermediate alleles and microRNA dysregulation to enhanced tauopathy in Late-Onset Alzheimer's DiseaseDOI 10.21203/rs.3.rs-7621820/v1Read

Connecting HTT intermediate alleles and microRNA dysregulation to enhanced tauopathy in late-onset Alzheimer's disease.Semantic proximity Read

Synergistic impact of CAG intermediate alleles in theHTTgene and microRNA dysregulation exacerbates spliceosome impairment and accelerates Tau pathology in the caudate nucleus of late-onset Alzheimer’s diseaseSemantic proximity Read

[The role of alleles with an intermediate number of trinucleotide repeats in Parkinson's disease and other neurodegenerative disorders].Semantic proximity Read

A dementia-associated risk variant near TMEM106B alters chromatin architecture and gene expressionSemantic proximity Read

Somatic CAG repeat instability in intermediate alleles of the HTT gene and its potential association with a clinical phenotype.Semantic proximity Read

Somatic CAG repeat expansion in blood associates with biomarkers of neurodegeneration in Huntington’s disease decades before clinical motor diagnosisSemantic proximity Read

Huntingtin CAG repeat is a continuous modifier of brain structure and health vulnerabilitySemantic proximity Read

Tau splicing and the intricacies of dementiaSemantic proximity Read

Tau isoform imbalance and aggregation are pathological hallmarks of X-linked dystonia-parkinsonismSemantic proximity Read

A new non-aggregative splicing isoform of human Tau is decreased in Alzheimer’s diseaseSemantic proximity Read

Prevalence of Carriers of Intermediate and Pathological Polyglutamine Disease–Associated Alleles Among Large Population-Based CohortsSemantic proximity Read

Multimodal spatial transcriptomics determines repeat expansion, huntingtin aggregation, and selective cortical neuron loss in Huntington’s DiseaseSemantic proximity Read