ArticleJournal of molecular neuroscience : MN2025
Association of Alzheimer's-Related Gene Variants with Autism Spectrum Disorder: A Case-Control Study in an Iraqi Cohort.
Article in Journal of molecular neuroscience : MN, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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
2 citing papers in PubMed.
- Pro-inflammatory Immune Dysregulation and Genetic Susceptibility in Iraqi Children with Autism: a Tetra-Primer ARMS-PCR Investigation of Interleukin Polymorphisms.Journal of molecular neuroscience : MN · 2026Article
- Pathophysiologic similarities between autism spectrum disorder and Alzheimer's disease: therapeutic possibilities.Frontiers in neuroscience · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Autism spectrum disorder (ASD) is a neurodevelopmental disorder that manifests as difficulties in social communication and the presence of restricted and repetitive behaviors. The etiology remains obscure, although there is increasing evidence of shared neurodevelopmental and neurodegenerative disorder pathways. This study aimed to determine whether gene variants previously linked to Alzheimer's disease (AD) have a role in ASD susceptibility. Within a case-control framework, we studied a sample of 270 Iraqi children, 135 with ASD and 135 age-matched controls aged 6-12 years. T-ARMS PCR was used to determine the genotypes of five selected polymorphisms NECTIN2 (rs6859), CR1 (rs670173), CLU (rs7982), ABCA7 (rs3764650), and BIN1 (rs744373) that have been associated with AD. The polymorphism genotype and allele frequencies were analyzed using the chi-square test, and odds ratio analysis with 95% confidence intervals was conducted. Age and sex-stratified analyses in addition to biochemical profiling were also conducted. Significant associations with ASD were found for three polymorphisms: CR1 rs670173 (p = 0.007), CLU rs7982 (p = 0.010), and BIN1 rs744373 (p = 0.013). The male-to-female effect ratio was stronger than the female-to-male. Interestingly, younger boys aged 6 to 9 years demonstrated the most pronounced effect of CLU rs7982 (OR = 1.92, 95% CI: 1.25-2.94, p = 0.003). NECTIN2 rs6859 (p = 0.543) and ABCA7 rs3764650 (p = 0.102) did not yield significant associations. Biochemical parameters showed no significant differences among the groups. Our results imply that some AD-associated gene variants, especially those related to neuroinflammation and synaptic activity, could elevate the risk for ASD. This reinforces the notion of shared genetic risk factors between neurodevelopmental and neurodegenerative disorders, likely involving common mechanisms for the formation and maintenance of neural circuits.
Indexed as
Identifiers
40327194What Socratic 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 Socratic graph.