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

Thiamine deficiency induces oxidative stress and exacerbates the plaque pathology in Alzheimer's mouse model.

Neurobiology of aging - 1 Oct 2009

Karuppagounder Saravanan S, Xu Hui, Shi Qingli, Chen Lian H, Pedrini Steve, Pechman David, Baker Harriet, Beal M Flint, Gandy Sam E, Gibson Gary E

Abstract excerpt

Mitochondrial dysfunction, oxidative stress and reductions in thiamine-dependent enzymes have been implicated in multiple neurological disorders including Alzheimer's disease (AD). Experimental thiamine deficiency (TD) is an established model for reducing the activities of thiamine-dependent enzymes in brain. TD diminishes thiamine-dependent enzymes throughout the brain, but produces a time-dependent selective...

Read the complete abstract on PubMed

Topics

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

Share to Amyloid beta-Peptides
Share to Amyloid beta-Protein Precursor

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Amyloid Precursor Protein Secretases

Share to Aspartic Acid Endopeptidases

Share to Neuroglia

Share to Peptide Fragments

Share to Plaque, Amyloid

Share to Receptors, Cell Surface

Source

Open in PubMed Open full text

Identifiers

PMID: 18406011
DOI: 10.1016/j.neurobiolaging.2007.12.013
PMCID: PMC2782730

Genes

APP
BACE1

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-08.1.

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

Thiamine deficiency induces oxidative stress and exacerbates the plaque pathology in Alzheimer's mouse model.PMID 18406011Read ↗

Elevated levels of brain homocysteine directly modulate the pathological phenotype of a mouse model of tauopathy.Semantic proximity Read ↗

Tau protein aggregation induces cellular senescence in the brainSemantic proximity Read ↗

Tau protein aggregation is associated with cellular senescence in the brainSemantic proximity Read ↗

Deletion of vitamin E enhances phenotype of Alzheimer disease model mouse.Semantic proximity Read ↗

Oxidative Stress during the Progression of β-Amyloid Pathology in the Neocortex of the Tg2576 Mouse Model of Alzheimer's Disease.Semantic proximity Read ↗

Changes in lipid metabolism track with the progression of neurofibrillary pathology in tauopathiesSemantic proximity Read ↗

Thiamine pyrophosphokinase-1 deficiency in neurons drives Alzheimer’s multiple pathophysiological alterationsSemantic proximity Read ↗

Homocysteine exacerbates β-amyloid pathology, tau pathology, and cognitive deficit in a mouse model of Alzheimer disease with plaques and tangles.Semantic proximity Read ↗

Impaired Cu/Zn-SOD activity contributes to increased oxidative damage in APP transgenic mice.Semantic proximity Read ↗

Neuroinflammation regulates the balance between hippocampal neuron death and neurogenesis in an ex vivo model of thiamine deficiencySemantic proximity Read ↗

Time sequence of oxidative stress in the brain from transgenic mouse models of Alzheimer's disease related to the amyloid-β cascade.Semantic proximity Read ↗

Reduction of the RNA Binding Protein TIA1 Exacerbates Neuroinflammation in TauopathySemantic proximity Read ↗

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