Childhood ADHD and subthreshold symptoms are associated with cognitive functioning at age 40-a cohort study on perinatal birth risks.

Introduction: In this prospective cohort study over 40 years we investigated the effect of childhood attention-deficit/hyperactivity disorder (ADHD) and subthreshold ADHD on cognitive performance in adulthood.

Methods: The cohort comprised individuals with mild perinatal risks. Childhood ADHD group (cADHD,  = 39) was compared to a group with subthreshold childhood attention or hyperactivity symptoms (cAP;  = 79), a group with similar perinatal risks but no ADHD symptoms ( = 255), and to controls without ADHD symptoms or perinatal risks ( = 69).

Childhood motor difficulties and cognitive impairment in midlife: A 40-year cohort study.

Objective: We aimed to examine the association of childhood motor difficulties (MD) with cognitive impairment in midlife.

Method: We studied 357 participants from a cohort born in 1971-1975. At age 9, they had completed the Test of Motor Impairment, which classified them into three groups: childhood MD (cMD), borderline cMD (bcMD), or no cMD.

The shared ancestry between the C9orf72 hexanucleotide repeat expansion and intermediate-length alleles using haplotype sharing trees and HAPTK.

The C9orf72 hexanucleotide repeat expansion (HRE) is a common genetic cause of amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD). The inheritance is autosomal dominant, but a high proportion of subjects with the mutation are simplex cases. One possible explanation is de novo expansions of unstable intermediate-length alleles (IAs).

Motor difficulties from childhood to midlife: A 40-year cohort study.

Background: There are few studies of the persistence of childhood motor difficulties (MD) into adulthood.

Aims: To investigate the association of childhood MD with motor skills and body mass index (BMI) in midlife.

Methods And Procedures: We studied 324 adults aged 40 from a cohort born in 1971-1974.

hexanucleotide repeat allele tagging SNPs: Associations with ALS risk and longevity.

hexanucleotide repeat expansion is a common cause of amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD). The locus may harbor residual risk outside the hexanucleotide repeat expansion, but the evidence is conflicting. Here, we first compared 683 unrelated amyotrophic lateral sclerosis cases and 3,196 controls with Finnish ancestry to find best single nucleotide polymorphisms that tag the hexanucleotide repeat expansion and intermediate-length alleles.