ReviewCurrent Alzheimer research2013
Is amyloid binding alcohol dehydrogenase a drug target for treating Alzheimer's disease?
Review in Current Alzheimer research, 2013. 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, 31 citations in OpenAlex.
- The inhibitors of 17β-HSD10: are they any good?RSC chemical biology · 2026Review
- Mitochondrial Transportation, Transplantation, and Subsequent Immune Response in Alzheimer's Disease: An Update.Molecular neurobiology · 2024Review
- Infantile Neurodegeneration Results from Mutants of 17β-Hydroxysteroid Dehydrogenase Type 10 Rather Than Aβ-Binding Alcohol Dehydrogenase.International journal of molecular sciences · 2023Review
- Rhein Relieves Oxidative Stress in an AβFrontiers in pharmacology · 2021Article
- Knockdown of HSDL2 inhibits lung adenocarcinoma progression via down-regulating AKT2 expression.Bioscience reports · 2020Observational
- Overexpression of endophilin A1 exacerbates synaptic alterations in a mouse model of Alzheimer's disease.Nature communications · 2018Article
- Role of Hydroxysteroid Dehydrogenase-Like 2 (HSDL2) in Human Ovarian Cancer.Medical science monitor : international medical journal of experimental and clinical research · 2018Article
- A Mitocentric View of Alzheimer's Disease.Molecular neurobiology · 2017Review
- Physiological and pathophysiological functions of Swiprosin-1/EFhd2 in the nervous system.The Biochemical journal · 2016Review
- Lipids and Oxidative Stress Associated with Ethanol-Induced Neurological Damage.Oxidative medicine and cellular longevity · 2016Review
- Key Targets for Multi-Target Ligands Designed to Combat Neurodegeneration.Frontiers in neuroscience · 2016Review
- Myxococcus CsgA, Drosophila Sniffer, and human HSD10 are cardiolipin phospholipases.Genes & development · 2015Article
- Auto-inhibitory Mechanism of the Human Mitochondrial RNase P Protein Complex.Scientific reports · 2015Article
- Alzheimer's pathogenesis and its link to the mitochondrion.Oxidative medicine and cellular longevity · 2015Review
- Osteoporosis and alzheimer pathology: Role of cellular stress response and hormetic redox signaling in aging and bone remodeling.Frontiers in pharmacology · 2014Review
- Article
- The novel amyloid-beta peptide aptamer inhibits intracellular amyloid-beta peptide toxicity.Neural regeneration research · 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
6 authors at 3 institutions in 3 countries.
Funding
Abstract
Current strategies for the treatment of Alzheimer's disease (AD) involve tackling the formation or clearance of the amyloid-beta peptide (Aβ) and/or hyper-phosphorylated tau, or the support and stabilization of the remaining neuronal networks. However, as we gain a clearer idea of the large number of molecular mechanisms at work in this disease, it is becoming clearer that the treatment of AD should take a combined approach of dealing with several aspects of the pathology. The concept that we also need to protect specific sensitive targets within the cell should also be considered. In particular the role of protecting the function of a specific mitochondrial protein, amyloid binding alcohol dehydrogenase (ABAD), will be the focus of this review. Mitochondrial dysfunction is a well-recognized fact in the progression of AD, though until recently the mechanisms involved could only be loosely labeled as changes in 'metabolism'. The discovery that Aβ can be present within the mitochondria and specifically bind to ABAD, has opened up a new area of AD research. Here we review the evidence that the prevention of Aβ binding to ABAD is a drug target for the treatment of AD.
Indexed as
Identifiers
22742981PMC3674883W2102162464What 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.