ArticleCurrent genomics2013
Role of the Transforming-Growth-Factor-β1 Gene in Late-Onset Alzheimer's Disease: Implications for the Treatment.
Article in Current genomics, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 39 citations in OpenAlex.
- Alzheimer's Disease: From Molecular Mechanisms to Promising Therapeutic Strategies.International journal of molecular sciences · 2025Review
- Tracking neuroinflammatory biomarkers in Alzheimer's disease: a strategy for individualized therapeutic approaches?Journal of neuroinflammation · 2024Review
- Specific exercise patterns generate an epigenetic molecular memory window that drives long-term memory formation and identifies ACVR1C as a bidirectional regulator of memory in mice.Nature communications · 2024Article
- Aging Microglia and Their Impact in the Nervous System.Advances in neurobiology · 2024Review
- Behavioral and neuropathological features of Alzheimer's disease are attenuated in 5xFAD mice treated with intranasal GHK peptide.Aging pathobiology and therapeutics · 2024Article
- Intranasal GHK peptide enhances resilience to cognitive decline in aging mice.bioRxiv : the preprint server for biology · 2023Article
- Cellular Localization and Distribution of TGF-β1, GDNF and PDGF-BB in the Adult Primate Central Nervous System.Neurochemical research · 2023Article
- Discovery of novel CSF biomarkers to predict progression in dementia using machine learning.Scientific reports · 2023Article
- TGF-β1 signalling in Alzheimer's pathology and cytoskeletal reorganization: a specialized Tau perspective.Journal of neuroinflammation · 2023Review
- Allopregnanolone pleiotropic action in neurons and astrocytes: calcium signaling as a unifying mechanism.Frontiers in endocrinology · 2023Article
- The Therapeutic Potential of Carnosine/Anserine Supplementation against Cognitive Decline: A Systematic Review with Meta-Analysis.Biomedicines · 2021Article
- Neuroprotective activity ofHeliyon · 2020Article
- TGF-β Signaling: A Therapeutic Target to Reinstate Regenerative Plasticity in Vascular Dementia?Aging and disease · 2020Review
- Prediction of Alzheimer's disease using blood gene expression data.Scientific reports · 2020Article
- Gender-Specific Differences in Concentrations of Biochemical Parameters in Persons over the Age of 90.International journal of environmental research and public health · 2019Article
- Age and Age-Related Diseases: Role of Inflammation Triggers and Cytokines.Frontiers in immunology · 2018Review
- Suppression of Transforming Growth Factor-β Signaling Delays Cellular Senescence and Preserves the Function of Endothelial Cells Derived from Human Pluripotent Stem Cells.Stem cells translational medicine · 2017Article
- NeuroRDF: semantic integration of highly curated data to prioritize biomarker candidates in Alzheimer's disease.Journal of biomedical semantics · 2016Article
- Brain-Derived Neurotrophic Factor in Alzheimer's Disease: Risk, Mechanisms, and Therapy.Molecular neurobiology · 2015Article
- Role of TGFβ signaling in the pathogenesis of Alzheimer's disease.Frontiers in cellular neuroscience · 2015Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Late-onset Alzheimer's disease (LOAD) is the most common form of dementia in the elderly. LOAD has a complex and largely unknown etiology with strong genetic determinants. Genetics of LOAD is known to involve several genetic risk factors among which the Apolipoprotein E (APOE) gene seems to be the major recognized genetic determinant. Recent efforts have been made to identify other genetic factors involved in the pathophysiology of LOAD such as genes associated with a deficit of neurotrophic factors in the AD brain. Genetic variations of neurotrophic factors, such as brain-derived neurotrophic factor (BDNF), and transforming-growth-factor-β1 (TGF-β1) are known to increase the risk to develop LOAD and have also been related to depression susceptibility in LOAD. Transforming-Growth-Factor-β1 (TGF-β1) is a neurotrophic factor that exerts neuroprotective effects against ß-amyloid-induced neurodegeneration. Recent evidence suggests that a specific impairment in the signaling of TGF-β is an early event in the pathogenesis of AD. TGF-β1 protein levels are predominantly under genetic control, and the TGF-β1 gene, located on chromosome 19q13.1-3, con-tains several single nucleotide polymorphisms (SNPs) upstream and in the transcript region, such as the SNP at codon +10 (T/C) and +25 (G/C), which is known to influence the level of expression of TGF-β1. In the present review, we summarize the current literature on genetic risk factors for LOAD, focusing on the role of the TGF-β1 gene, finally discussing the possible implications of these genetic studies for the selection of patients eligible for neuroprotective strategies in AD.
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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.