Developmental disorders of language include developmental language disorder, dyslexia, and motor-speech disorders such as articulation disorder and stuttering. These disorders have generally been explained by accounts that focus on their behavioral rather than neural characteristics; their processing rather than learning impairments; and each disorder separately rather than together, despite their commonalities and comorbidities. Here we update and review a unifying neurocognitive account-the Procedural circuit Deficit Hypothesis (PDH). The PDH posits that abnormalities of brain structures underlying procedural memory (learning and memory that rely on the basal ganglia and associated circuitry) can explain numerous brain and behavioral characteristics across learning and processing, in multiple disorders, including both commonalities and differences. We describe procedural memory, examine its role in various aspects of language, and then present the PDH and relevant evidence across language-related disorders. The PDH has substantial explanatory power, and both basic research and translational implications.
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http://dx.doi.org/10.1146/annurev-psych-122216-011555 | DOI Listing |
Eur Child Adolesc Psychiatry
January 2025
School of Psychology, Centre for Innovation in Mental Health, University of Southampton, University Road, Southampton, SO17 1BJ, UK.
The directionality of the relationship between adolescent alcohol consumption and mental health difficulties remains poorly understood. This study investigates the longitudinal relationship between alcohol use frequency, internalizing and externalizing symptoms from the ages of 11 to 17. We conducted a random-intercept cross-lagged panel model across three timepoints (ages: 11yrs, 14yrs, 17yrs; 50.
View Article and Find Full Text PDFSci China Life Sci
January 2025
Department of Cell Biology, School of Basic Medical Sciences, Peking University Stem Cell Research Center, Peking University Health Science Center, Peking University, Beijing, 100191, China.
Human primed pluripotent stem cells are capable of generating all the embryonic lineages. However, their extraembryonic trophectoderm potentials are limited. It remains unclear how to expand their developmental potential to trophectoderm lineages.
View Article and Find Full Text PDFProg Mol Biol Transl Sci
January 2025
Genetics & Developmental Biology Laboratory, Department of Biotechnology & Bioengineering, Institute of Advanced Research, Gandhinagar, Gujarat, India. Electronic address:
Different neurological diseases including, Parkinson's, Alzheimer's, and Huntington's diseases extant momentous global disease burdens, affecting millions of lives for imposing a heavy disease burden on the healthcare systems. Despite various treatment strategies aimed at alleviating symptoms, treatments remain elusive and ineffective due to the disease's complexity. However, recent advancements in gene therapy via the CRISPR-Cas system offer ground-breaking and targeted treatment options.
View Article and Find Full Text PDFMol Biol Evol
January 2025
Bio-X Institutes, Key Laboratory for the Genetics of Developmental and Neuropsychiatric Disorders, Ministry of Education, Shanghai Jiao Tong University, Shanghai 200240, China.
5-methylation (m5C) on mRNA molecules is a prevalent internal posttranscriptional modification in eukaryotes. Although m5C modification has been reported to regulate some biological processes, it is unknown whether most mRNA m5C modifications are functional. To address this question, we analyzed the genome-wide evolutionary characteristics of m5C modifications in protein-coding genes of humans and mice.
View Article and Find Full Text PDFAm J Hum Genet
January 2025
Institute of Medical Genetics and Applied Genomics, University of Tübingen, Tübingen, Germany; Center for Rare Disease, University of Tübingen, Tübingen, Germany; Genomics for Health in Africa (GHA), Africa-Europe Cluster of Research Excellence (CoRE). Electronic address:
Nutrient-dependent mTORC1 regulation upon amino acid deprivation is mediated by the KICSTOR complex, comprising SZT2, KPTN, ITFG2, and KICS2, recruiting GATOR1 to lysosomes. Previously, pathogenic SZT2 and KPTN variants have been associated with autosomal recessive intellectual disability and epileptic encephalopathy. We identified bi-allelic KICS2 variants in eleven affected individuals presenting with intellectual disability and epilepsy.
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