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Anhedonia is increasingly recognized as a transdiagnostic risk factor for psychopathology. New evidence demonstrates that anhedonia is present in infancy and early childhood. Structural variability in striatal regions involved in reward processing and pleasure seeking is concurrently linked to anhedonia, yet few studies have examined whether striatal differences presage anhedonia, and none have examined prospective associations before middle childhood. The present study examined whether neuroanatomical markers that confer risk for anhedonia can be detected as early as the neonatal period. Specifically, we tested whether the volume of striatal regions in neonates predicted the emergence of infant anhedonic behaviors at six months of age. Our sample included 89 neonates (47 females, 42 males) from the Care Project - a longitudinal cohort study of pregnant individuals and their children. Neonatal striatal volume (nucleus accumbens, putamen, and caudate) was assessed using structural magnetic resonance imaging (MRI; M: 43 postconceptional weeks). Anhedonic behaviors were measured using the Infant Hedonic/Anhedonic Processing Index (HAPI-Infant) at six months. Larger neonatal nucleus accumbens (right: β = 0.32, p = .003; left: β = 0.22, p = .04) and putamen (right: β = 0.29, p = .03; left: β = 0.28, p = .04) volume predicted more anhedonic behaviors at six months, covarying for intracranial volume, postconceptional age at scan, sex at birth, and birth weight percentile. This study demonstrates that neonatal striatal volume is associated with anhedonia in infancy and provides the first evidence that markers of vulnerability to anhedonia can be detected in neonates.
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http://dx.doi.org/10.1016/j.jad.2025.120211 | DOI Listing |
J Affect Disord
September 2025
University of Denver, Department of Psychology, United States of America; University of California, Irvine, Department of Pediatrics, United States of America. Electronic address:
Anhedonia is increasingly recognized as a transdiagnostic risk factor for psychopathology. New evidence demonstrates that anhedonia is present in infancy and early childhood. Structural variability in striatal regions involved in reward processing and pleasure seeking is concurrently linked to anhedonia, yet few studies have examined whether striatal differences presage anhedonia, and none have examined prospective associations before middle childhood.
View Article and Find Full Text PDFZhen Ci Yan Jiu
July 2025
College of Acupuncture-moxibustion, Tuina and Rehabilitation, Hunan University of Traditional Chinese Medicine, Changsha 410208, China.
Objectives: To observe the effect of acupuncture on the expression of brain-derived neurotrophic factor (BDNF), tyrosine kinase receptor B (TrkB), extracellular signal-regulated kinase (ERK), cyclic adenosine monophosphate (cAMP)-response element binding protein (CREB), as well as synapsin1 (Syn1) and synaptophysin (Syp) in the striatum of neonatal rats with hypoxic-ischemic brain damage ( HIBD), so as to explore its mechanisms underlying improvement of motor control.
Methods: Seven-day-old neonatal SD rats were randomly and equally assigned to 4 groups:blank control, sham-operation, model, and acupuncture groups (=12 per group) according to the randomized numerical table method. The HIBD model was established by using modified Rice's method.
Sci Rep
July 2025
Department of Biological Sciences, Clemson University, Clemson, SC, 29634-0314, USA.
Neural stem cells (NSCs) of the ventricular-subventricular zone (V-SVZ) generate diverse cell types including striatal glia during the neonatal period. NSC progeny uncouple stem cell-related mRNA transcripts from being translated during differentiation. We previously demonstrated that Tsc2 inactivation, which occurs in the neurodevelopmental disorder Tuberous Sclerosis Complex (TSC), prevents this from happening.
View Article and Find Full Text PDFBrain Dev
August 2025
Department of Pediatrics, Kyorin University School of Medicine, Tokyo, Japan.
Background: In some countries, glutaric acidemia type 1 (GA1) is included in newborn screening (NBS) panels using tandem mass spectrometry (MS/MS) analysis of acylcarnitine. However, the low excretor phenotype of glutaric acidemia type 1 (LE-GA1) has been increasingly recognaized and may lead to false-negative NBS results and can be missed by urine organic acid and plasma acylcarnitine profile analyses.
Case: We report a case of LE-GA1 with an atypical imaging course.
Clin Epigenetics
June 2025
Faculty of Medicine and Faculty of Life Sciences, Institute of Biomedical Sciences (ICB), Universidad Andres Bello, Santiago, Chile.
Background: Huntington's disease (HD) is an incurable hereditary disorder caused by an expansion of CAG repeats in exon 1 of the Huntingtin gene (HTT). HD is characterized by motor dysfunction and cognitive decline. The pathophysiology of HD begins in cortico-striatal circuits and later spreads to other brain regions, notably the hippocampus.
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