ArticleJournal of Alzheimer's disease : JAD2015
Genetic determinants of disease progression in Alzheimer's disease.
Article in Journal of Alzheimer's disease : JAD, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers, 4 of them syntheses that pooled it.
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
35 citing papers in PubMed, 4 syntheses or guidelines pooled it, 63 citations in OpenAlex.
- Targeting TREM2 for Parkinson's Disease: Where to Go?Frontiers in immunology · 2021Pooled it
- INPP5D rs35349669 polymorphism with late-onset Alzheimer's disease: A replication study and meta-analysis.Oncotarget · 2016Pooled it
- MEF2C rs190982 polymorphism with late-onset Alzheimer's disease in Han Chinese: A replication study and meta-analyses.Oncotarget · 2016Pooled it
- ZCWPW1 is associated with late-onset Alzheimer's disease in Han Chinese: a replication study and meta-analyses.Oncotarget · 2016Pooled it
- ADAM19: biological characteristics and implications in disease pathology and clinical applications.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Review
- Genetic Associations with Temporal Modeling of Alzheimer's Disease Progression Supports a Novel Paradigm for Disease Risk.medRxiv : the preprint server for health sciences · 2026Article
- Keeping up with the nicotinamides: NADP(H), the forgotten circadian cofactor that keeps metabolic time.Life metabolism · 2025Review
- Review
- Variant-to-function mapping of late-onset Alzheimer's disease GWAS signals in human microglial cell models implicatesbioRxiv : the preprint server for biology · 2024Article
- Association between MEF2 family gene polymorphisms and susceptibility to multiple sclerosis in Chinese population.Acta neurologica Belgica · 2024Article
- Alzheimer's Disease: Models and Molecular Mechanisms Informing Disease and Treatments.Bioengineering (Basel, Switzerland) · 2024Review
- Pathological Roles of INPP5D in Alzheimer's Disease.Advances in experimental medicine and biology · 2023Article
- TREM2 risk variants are associated with atypical Alzheimer's disease.Acta neuropathologica · 2022Article
- Review
- Astrocytes as a Therapeutic Target in Alzheimer's Disease-Comprehensive Review and Recent Developments.International journal of molecular sciences · 2022Review
- Association of rs3027178 polymorphism in the circadian clock gene PER1 with susceptibility to Alzheimer's disease and longevity in an Italian population.GeroScience · 2022Article
- Deep learning algorithm reveals probabilities of stage-specific time to conversion in individuals with neurodegenerative disease LATE.Alzheimer's & dementia (New York, N. Y.) · 2022Article
- Identification of a novel mutation in MEF2C gene in an atypical patient with frontotemporal lobar degeneration.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2022Article
- Machine Learning Approach Predicts Probability of Time to Stage-Specific Conversion of Alzheimer's Disease.Journal of Alzheimer's disease : JAD · 2022Article
- Fine Particle Exposure and Clinical Aggravation in Neurodegenerative Diseases in New York State.Environmental health perspectives · 2021Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
There is a strong genetic basis for late-onset Alzheimer's disease (LOAD); thus far 22 genes/loci have been identified that affect the risk of LOAD. However, the relationships among the genetic variations at these loci and clinical progression of the disease have not been fully explored. In the present study, we examined the relationships of 22 known LOAD genes to the progression of AD in 680 AD patients recruited from the University of Pittsburgh Alzheimer's Disease Research Center. Patients were classified as "rapid progressors" if the Mini-Mental State Examination (MMSE) changed ≥3 points in 12 months and "slow progressors" if the MMSE changed ≤2 points. We also performed a genome-wide association study in this cohort in an effort to identify new loci for AD progression. Association analysis between single nucleotide polymorphisms (SNPs) and the progression status of the AD cases was performed using logistic regression model controlled for age, gender, dementia medication use, psychosis, and hypertension. While no significant association was observed with either APOE*4 (p = 0.94) or APOE*2 (p = 0.33) with AD progression, we found multiple nominally significant associations (p < 0.05) either within or adjacent to seven known LOAD genes (INPP5D, MEF2C, TREM2, EPHA1, PTK2B, FERMT2, and CASS4) that harbor both risk and protective SNPs. Genome-wide association analyses identified four suggestive loci (PAX3, CCRN4L, PIGQ, and ADAM19) at p < 1E-05. Our data suggest that short-term clinical disease progression in AD has a genetic basis. Better understanding of these genetic factors could help to improve clinical trial design and potentially affect the development of disease modifying therapies.
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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.