ReviewNeuroscience2009
Endophenotypes in normal brain morphology and Alzheimer's disease: a review.
Review in Neuroscience, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 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
23 citing papers in PubMed, 50 citations in OpenAlex.
- Article
- Multivariate genome-wide association study of depression, cognition, and memory phenotypes and validation analysis identify 12 cross-ethnic variants.Translational psychiatry · 2022Article
- Early-Life Environment Influence on Late-Onset Alzheimer's Disease.Frontiers in cell and developmental biology · 2022Review
- Article
- Imaging Genetics in Epilepsy: Current Knowledge and New Perspectives.Frontiers in molecular neuroscience · 2022Review
- Association of low-frequency and rare coding variants with information processing speed.Translational psychiatry · 2021Article
- Thrombin and theFrontiers in neurology · 2019Review
- Early Life Stress and Epigenetics in Late-onset Alzheimer's Dementia: A Systematic Review.Current genomics · 2018Review
- Review
- Polygenic risk score: use in migraine research.The journal of headache and pain · 2018Review
- Attentional performance, impulsivity, and related neurotransmitter systems in apoE2, apoE3, and apoE4 female transgenic mice.Psychopharmacology · 2016Article
- Mitochondrial DNA deletions in Alzheimer's brains: a review.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2014Review
- Perspectives in molecular imaging using staging biomarkers and immunotherapies in Alzheimer's disease.TheScientificWorldJournal · 2013Review
- The paradox of syndromic diversity in Alzheimer disease.Nature reviews. Neurology · 2012Review
- TOMM40 poly-T repeat lengths, age of onset and psychosis risk in Alzheimer disease.Neurobiology of aging · 2011Article
- Neuropsychiatric Symptoms, Endophenotypes, and Syndromes in Late-Onset Alzheimer's Disease: Focus on APOE Gene.International journal of Alzheimer's disease · 2011Article
- CR1 is associated with amyloid plaque burden and age-related cognitive decline.Annals of neurology · 2011Article
- The apolipoprotein e antagonistic pleiotropy hypothesis: review and recommendations.International journal of Alzheimer's disease · 2011Article
- Micro soft tissues visualization based on x-ray phase-contrast imaging.The open medical informatics journal · 2011Article
- Impact of SORL1 single nucleotide polymorphisms on Alzheimer's disease cerebrospinal fluid markers.Dementia and geriatric cognitive disorders · 2011Article
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
Abstract
Late-onset Alzheimer's disease is a common complex disorder of old age. Though these types of disorders can be highly heritable, they differ from single-gene (Mendelian) diseases in that their causes are often multifactorial with both genetic and environmental components. Genetic risk factors that have been firmly implicated in the cause are mutations in the amyloid precursor protein (APP), presenilin 1 (PSEN1) and presenilin 2 (PSEN2) genes, which are found in large multi-generational families with an autosomal dominant pattern of disease inheritance, the apolipoprotein E (APOE)epsilon4 allele and the sortilin-related receptor (SORL1) gene. Environmental factors that have been associated with late-onset Alzheimer's disease include depressive illness, various vascular risk factors, level of education, head trauma and estrogen replacement therapy. This complexity may help explain their high prevalence from an evolutionary perspective, but the etiologic complexity makes identification of disease-related genes much more difficult. The "endophenotype" approach is an alternative method for measuring phenotypic variation that may facilitate the identification of susceptibility genes for complexly inherited traits. The usefulness of endophenotypes in genetic analyses of normal brain morphology and, in particular for Alzheimer's disease will be reviewed as will the implications of these findings for models of disease causation. Given that the pathways from genotypes to end-stage phenotypes are circuitous at best, identifying endophenotypes more proximal to the effects of genetic variation may expedite the attempts to link genetic variants to disorders.
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.