ArticleDialogues in clinical neuroscience2003
Genetic studies in Alzheimer's disease.
Article in Dialogues in clinical neuroscience, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
What it found
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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
18 citing papers in PubMed, 49 citations in OpenAlex.
- Mitochondria-Targeted Nanotherapies in Aging Neurodegenerative Disorders: Emerging Prospects and Clinical Potential.Advanced healthcare materials · 2026Review
- Transcriptional Landscape and Biomarker Discovery for Endoplasmic Reticulum Stress in Alzheimer's Disease: An Ex Vivo Study Using Patients-Derived Dermal Fibroblasts.Psychiatry investigation · 2025Article
- Alzheimer's Disease: Exploring the Landscape of Cognitive Decline.ACS chemical neuroscience · 2024Review
- APP in the Neuromuscular Junction for the Development of Sarcopenia and Alzheimer's Disease.International journal of molecular sciences · 2023Review
- Obesity reduces hippocampal structure and function in older African Americans with the APOE-ε4 Alzheimer's disease risk allele.Frontiers in aging neuroscience · 2023Article
- Prediction of Translational Regulation by Network Interaction in Synaptic Plasticity Induced withTheScientificWorldJournal · 2023Article
- 1-L Transcription in Alzheimer's Disease.Current issues in molecular biology · 2022Article
- A Quantitative Model of Sporadic Axonal Degeneration in theThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2022Article
- Review
- Green Tea Seed Isolated Theasaponin E1 Ameliorates AD Promoting Neurotoxic Pathogenesis by Attenuating Aβ Peptide Levels in SweAPP N2a Cells.Molecules (Basel, Switzerland) · 2020Article
- What's That (Blue) Spot on my MRI? Multimodal Neuroimaging of the Locus Coeruleus in Neurodegenerative Disease.Frontiers in neuroscience · 2020Review
- Identification of Dysregulated Genes for Late-Onset Alzheimer's Disease Using Gene Expression Data in Brain.Journal of Alzheimer's disease & Parkinsonism · 2020Article
- Biological and Cognitive Markers of Presenilin1 E280A Autosomal Dominant Alzheimer's Disease: A Comprehensive Review of the Colombian Kindred.The journal of prevention of Alzheimer's disease · 2019Review
- Targeting Autophagy for the Treatment of Alzheimer's Disease: Challenges and Opportunities.Frontiers in molecular neuroscience · 2019Article
- Effects of medicinal plants on Alzheimer's disease and memory deficits.Neural regeneration research · 2017Review
- Autophagy and Alzheimer's Disease.Cellular and molecular neurobiology · 2017Review
- Rodent models for Alzheimer's disease drug discovery.Expert opinion on drug discovery · 2015Review
- Three-dimensional structure of human γ-secretase.Nature · 2014Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Alzheimer's disease (AD), the most common cause of dementia in aged populations, is believed to be caused by both environmental factors and genetic variations. Extensive linkage and association studies have established that a broad range of loci are associated with AD, including both causative and susceptibility (risk factor) genes. So far, at least three genes, APP, PS1, and PS2, have been identified as causative genes. Mutations in these genes have been found to cause mainly early-onset AD. On the other hand, APOE has been identified to be the most common high genetic risk factor for late-onset AD. Polymorphisms in the coding region, intron, and promoter region of certain genes constitute another kind of genetic variation associated with AD. A number of other genes or loci have been reported to have linkage with AD, but many show only a weak linkage or the results are not well reproduced. Currently, the measurable genetic associations account for about 50% of the population risk for AD. It is believed that more new loci will be found to associate with AD, either as causative genes or genetic risk factors, and that eventually the understanding of genetic factors in the pathogenesis of AD will be important for our efforts to cure this illness.
Indexed as
Identifiers
22033785PMC3181712W2126570001What 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.