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

Combined expression of tau and the Harlequin mouse mutation leads to increased mitochondrial dysfunction, tau pathology and neurodegeneration.

Neurobiology of aging - 1 Oct 2011

Kulic Luka, Wollmer M Axel, Rhein Virginie, Pagani Lucia, Kuehnle Katrin, Cattepoel Susann, Tracy Jay, Eckert Anne, Nitsch Roger M

Abstract excerpt

Mitochondrial dysfunction and oxidative stress play an important role in ageing and have been implicated in several age-related neurodegenerative conditions including Alzheimer's disease (AD) and other tauopathies characterized by the presence of intracellular accumulations of the hyperphosphorylated microtubule-associated protein tau. To study the interaction between mitochondrial dysfunction and tau pathology...

Read the complete abstract on PubMed

Topics

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

Share to Caspase 3
Share to Electron Transport Complex I

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to In Situ Nick-End Labeling

Share to Lipid Peroxidation

Share to Movement Disorders

Share to Proton Pumps

Share to Silver Staining

Share to Tauopathies

Source

Identifiers

PMID: 19942317
DOI: 10.1016/j.neurobiolaging.2009.10.014

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

Combined expression of tau and the Harlequin mouse mutation leads to increased mitochondrial dysfunction, tau pathology and neurodegeneration.PMID 19942317Read ↗

Increased mtDNA mutations with aging promotes amyloid accumulation and brain atrophy in the APP/Ld transgenic mouse model of Alzheimer's disease.Semantic proximity Read ↗

Relationship between Cognitive Dysfunction and Age-Related Variability in Oxidative Markers in Isolated Mitochondria of Alzheimer’s Disease Transgenic Mouse BrainsSemantic proximity Read ↗

Early Mitochondrial Defects in the 5xFAD mouse model of Alzheimer’s DiseaseSemantic proximity Read ↗

Convergence of Amyloid-β and Tau Pathologies on Mitochondria In VivoSemantic proximity Read ↗

Apoptosis-Inducing Factor Deficiency Induces Early Mitochondrial Degeneration in Brain Followed by Progressive Multifocal NeuropathologySemantic proximity Read ↗

Genetic mouse models of brain ageing and Alzheimer's disease.Semantic proximity Read ↗

The harlequin mouse mutation downregulates apoptosis-inducing factor.Semantic proximity Read ↗

Mitochondrial dysfunction induced by disease relevant AbetaPP and tau protein mutations.Semantic proximity Read ↗

Mitochondrial amyloid-beta levels are associated with the extent of mitochondrial dysfunction in different brain regions and the degree of cognitive impairment in Alzheimer's transgenic mice.Semantic proximity Read ↗

Mitochondrial perturbation drives tau oligomers pathology in Alzheimer’s diseaseSemantic proximity Read ↗

Mild deficiency of mitochondrial Complex III in a mouse model of Alzheimer’s disease decreases amyloid beta plaque formationSemantic proximity Read ↗

Increased mutation in mice genetically predisposed to oxidative damage in the brain.Semantic proximity Read ↗

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