ArticleNeurobiology of aging2012
ADAM10 expression and promoter haplotype in Alzheimer's disease.
Article in Neurobiology of aging, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 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
17 citing papers in PubMed, 30 citations in OpenAlex.
- Effects of BACE2 polymorphisms on verbal memory in the general population.European archives of psychiatry and clinical neuroscience · 2026Article
- GALM Alleviates Aβ Pathology and Cognitive Deficit Through Increasing ADAM10 Maturation in a Mouse Model of Alzheimer's Disease.Neuroscience bulletin · 2025Article
- Article
- Therapeutic potential of ADAM10 modulation in Alzheimer's disease: a review of the current evidence.Cell communication and signaling : CCS · 2023Review
- Stage-dependent involvement of ADAM10 and its significance in epileptic seizures.Journal of cellular and molecular medicine · 2019Review
- Exposure to fluoride aggravates the impairment in learning and memory and neuropathological lesions in mice carrying the APP/PS1 double-transgenic mutation.Alzheimer's research & therapy · 2019Article
- Regulation of ADAM10 by miR-140-5p and potential relevance for Alzheimer's disease.Neurobiology of aging · 2018Article
- Impact of ADAM10 gene polymorphisms on hepatocellular carcinoma development and clinical characteristics.International journal of medical sciences · 2018Article
- Influence of ADAM10 Polymorphisms on Plasma Level of Soluble Receptor for Advanced Glycation End Products and The Association With Alzheimer's Disease Risk.Frontiers in genetics · 2018Article
- Regulatory region genetic variation is associated with FYN expression in Alzheimer's disease.Neurobiology of aging · 2017Article
- Profiling microRNA from Brain by Microarray in a Transgenic Mouse Model of Alzheimer's Disease.BioMed research international · 2017Article
- Pathophysiological Function of ADAMTS Enzymes on Molecular Mechanism of Alzheimer's Disease.Aging and disease · 2016Review
- Promoter Variants of the ADAM10 Gene and Their Roles in Temporal Lobe Epilepsy.Frontiers in neurology · 2016Article
- Genetic association between APP, ADAM10 gene polymorphism, and sporadic Alzheimer's disease in the Chinese population.Neurotoxicity research · 2015Article
- An ADAM10 promoter polymorphism is a functional variant in severe sepsis patients and confers susceptibility to the development of sepsis.Critical care (London, England) · 2015Article
- Shedding the epilepsy comorbidity in Alzheimer's disease.Epilepsy currents · 2014Article
- An association study on ADAM10 promoter polymorphisms and atherosclerotic cerebral infarction in a Chinese population.CNS neuroscience & therapeutics · 2013Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors at 6 institutions in 1 country.
Funding
Abstract
Alzheimer's disease is confirmed at autopsy according to the accumulation of brain neuritic plaques and neurofibrillary tangles in the brain. Neuritic plaques contain amyloid-β (Aβ) and lower levels of Aβ correspond to an increase in ADAM10 α-secretase activity. ADAM10 α-secretase activity produces a soluble amyloid precursor protein (APP) alpha (sAPPα) product and negates the pathological production of Aβ. In this investigation, it was hypothesized that genetic variation with the ADAM10 promoter is associated with ADAM10 expression levels as well as cerebrospinal fluid sAPPα levels. Results from this investigation suggest that the ADAM10 rs514049-rs653765 C-A promoter haplotype is associated with: (1) higher CSF sAPPα levels in cognitively normal controls compared with Alzheimer's disease (AD) patients, (2) higher postmortem brain hippocampus, but not cerebellum, ADAM10 protein levels in subjects with low plaque scores compared with those with high plaque scores, and (3) higher promoter activity for promoter-only reporter constructs compared with promoter 3' untranslated region (3'UTR) constructs in the human neuroblastoma SHSY5Y cell line, but not in HepG2 or U118 cell lines. Taken together, these findings suggest that ADAM10 expression is modulated according to a promoter haplotype that is influenced in a brain region- and cell type-specific manner.
Indexed as
Identifiers
What 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.