ArticleInternational journal of clinical and experimental pathology2008
Tissue transglutaminase, protein cross-linking and Alzheimer's disease: review and views.
Article in International journal of clinical and experimental pathology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
26 citing papers in PubMed, 47 citations in OpenAlex.
- Transcriptional signatures related to glucose and lipid metabolism predict treatment response to the tumor necrosis factor antagonist infliximab in patients with treatment-resistant depression.Brain, behavior, and immunity · 2013Trial
- Biophysical assessment of the molecular mechanisms of Tau aggregation and its role in Alzheimer's disease.Protein science : a publication of the Protein Society · 2026Review
- Transglutaminase and its role in Alzheimer's disease: focus on mitochondria, aging, defective mitophagy, synaptic degeneration, and metabolomics.GeroScience · 2026Review
- Tauopathies: Calmodulin Regulates Tau Hyperphosphorylation and Its Transformation into Disease-Specific Aggregates.Biomolecules · 2025Review
- Polyamination with spermidine enhances pathogenic tau conformations while reducing filamentous aggregate formation in vitro.The Biochemical journal · 2025Article
- The Search for a Universal Treatment for Defined and Mixed Pathology Neurodegenerative Diseases.International journal of molecular sciences · 2024Review
- Absence of tissue transglutaminase reduces amyloid-beta pathology in APP23 mice.Neuropathology and applied neurobiology · 2022Article
- Oxidative Crosslinking of Peptides and Proteins: Mechanisms of Formation, Detection, Characterization and Quantification.Molecules (Basel, Switzerland) · 2021Review
- Overlapping Protein Accumulation Profiles of CADASIL and CAA: Is There a Common Mechanism Driving Cerebral Small-Vessel Disease?The American journal of pathology · 2021Review
- Structures of Human Transglutaminase 2: Finding Clues for Interference in Cross-linking Mediated Activity.International journal of molecular sciences · 2020Review
- Single-Domain Antibodies as Therapeutic and Imaging Agents for the Treatment of CNS Diseases.Antibodies (Basel, Switzerland) · 2019Review
- Effect of Some Growth Factors on Tissue Transglutaminase Overexpression Induced by β-Amyloid in Olfactory Ensheathing Cells.Molecular neurobiology · 2017Article
- The Aggregation Paths and Products of Aβ42 Dimers Are Distinct from Those of the Aβ42 Monomer.Biochemistry · 2016Article
- Catalytically active tissue transglutaminase colocalises with Aβ pathology in Alzheimer's disease mouse models.Scientific reports · 2016Article
- Emerging roles of sumoylation in the regulation of actin, microtubules, intermediate filaments, and septins.Cytoskeleton (Hoboken, N.J.) · 2015Review
- Cellular factors modulating the mechanism of tau protein aggregation.Cellular and molecular life sciences : CMLS · 2015Review
- Crystal structure of transglutaminase 2 with GTP complex and amino acid sequence evidence of evolution of GTP binding site.PloS one · 2014Article
- Different effects of soluble and aggregated amyloid β42 on gene/protein expression and enzyme activity involved in insulin and APP pathways.Journal of neural transmission (Vienna, Austria : 1996) · 2013Article
- Transglutaminase-2: a new endostatin partner in the extracellular matrix of endothelial cells.The Biochemical journal · 2010Article
- N-acetylcysteine prevents 4-hydroxynonenal- and amyloid-beta-induced modification and inactivation of neprilysin in SH-SY5Y cells.Journal of Alzheimer's disease : JAD · 2010Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Extensive protein cross-linking and aggregation are some of the most common molecular events in the pathogenesis of Alzheimer's disease (AD). Both beta-amyloid (Abeta) plaques and neurofibrillary tangles, which are extracellular and intracellular proteinaceous aggregates, respectively, contribute to neuronal death and progressive cognitive decline. Although protein cross-linking has been recognized and extensively studied for many years, the underlying mechanisms are largely unknown. Recent data indicates that tissue transglutaminase (tTG), which catalyzes the cross-linking of a wide spectrum of proteins including Abeta, tau, alpha-synuclein and neurofilament proteins, may be involved in protein aggregation in AD. Many AD risk factors, such as trauma, inflammation, ischemia and stress, up-regulate tTG protein and activity levels. In this review, we summarize the evidence that tTG plays a role in AD, especially in cross-linking of Abeta, tau, alpha-synuclein and neurofilament proteins. An experimentally testable hypothesis is that tTG may play a central role in AD pathogenesis and that it provides a conceptual link between sporadic and familial AD through a shared pathogenic pathway.
Indexed as
Identifiers
18784819PMC2480529W1509987864What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.