ArticleMolecular neurobiology2016
Tissue Transglutaminase and Its Product Isopeptide Are Increased in Alzheimer's Disease and APPswe/PS1dE9 Double Transgenic Mice Brains.
Article in Molecular neurobiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 25 citations in OpenAlex.
- Transglutaminase and its role in Alzheimer's disease: focus on mitochondria, aging, defective mitophagy, synaptic degeneration, and metabolomics.GeroScience · 2026Review
- Long non-coding RNAs potentially suppressive for brain perivascular astrogliosis induced by environmental ultrafine particulate matter.Environmental science and pollution research international · 2025Article
- Evaluation of mass spectrometry MS/MS spectra for the presence of isopeptide crosslinked peptides.PloS one · 2021Article
- Chlorpyrifos Oxon-Induced Isopeptide Bond Formation in Human Butyrylcholinesterase.Molecules (Basel, Switzerland) · 2020Article
- Cystamine and cysteamine as inhibitors of transglutaminase activityBioscience reports · 2018Review
- Religious Orders Study and Rush Memory and Aging Project.Journal of Alzheimer's disease : JAD · 2018Review
- Effect of Some Growth Factors on Tissue Transglutaminase Overexpression Induced by β-Amyloid in Olfactory Ensheathing Cells.Molecular neurobiology · 2017Article
- Inhibition of tissue transglutaminase promotes Aβ-induced apoptosis in SH-SY5Y cells.Acta pharmacologica Sinica · 2016Article
Corrections and comments
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Authors and funding
7 authors at 5 institutions in 2 countries.
Funding
Abstract
Alzheimer's disease (AD) is characterized by intracellular and extracellular protein aggregates, including microtubule-associated protein tau and cleavage product of amyloid precursor protein, β-amyloid (Aβ). Tissue transglutaminase (tTG) is a calcium-dependent enzyme that cross-links proteins forming a γ-glutamyl-ε-lysine isopeptide bond. Highly resistant to proteolysis, this bond can induce protein aggregation and deposition. We set out to determine if tTG may play a role in pathogenesis of AD. Previous studies have shown that tTG and isopeptide are increased in advanced AD, but they have not addressed if this is an early or late feature of AD. In the present study, we measured tTG expression levels and enzyme activity in the brains of individuals with no cognitive impairment (NCI), mild cognitive impairment (MCI), and AD, as well as a transgenic mouse model of AD. We found that both enzyme expression and activity were increased in MCI as well as AD compared to NCI. In the transgenic model of AD, tTG expression and enzyme activity increased sharply with age and were relatively specific for the hippocampus. We also assessed overlap of isopeptide immunoreactivity with neurodegeneration-related proteins with Western blots and found neurofilament, tau, and Aβ showed co-localization with isopeptide in both AD and transgenic mice. These results suggest that tTG might be a key factor in pathogenesis of abnormal protein aggregation in AD.
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Registered trials
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