Objective: While there has been considerable concern over possible adverse effects of psychostimulants on brain development, this issue has not been examined in a prospective study. The authors sought to determine prospectively whether psychostimulant treatment for attention deficit hyperactivity disorder (ADHD) was associated with differences in the development of the cerebral cortex during adolescence.
Method: Change in cortical thickness was estimated from two neuroanatomic MRI scans in 43 youths with ADHD. The mean age at the first scan was 12.5 years, and at the second scan, 16.4 years. Nineteen patients not treated with psychostimulants between the scans were compared with an age-matched group of 24 patients who were treated with psychostimulants. Further comparison was made against a template derived from 620 scans of 294 typically developing youths without ADHD.
Results: Adolescents taking psychostimulants differed from those not taking psychostimulants in the rate of change of the cortical thickness in the right motor strip, the left middle/inferior frontal gyrus, and the right parieto-occipital region. The group difference was due to more rapid cortical thinning in the group not taking psychostimulants (mean cortical thinning of 0.16 mm/year [SD=0.17], compared with 0.03 mm/year [SD=0.11] in the group taking psychostimulants). Comparison against the typically developing cohort without ADHD showed that cortical thinning in the group not taking psychostimulants was in excess of age-appropriate rates. The treatment groups did not differ in clinical outcome, however.
Conclusions: These findings show no evidence that psychostimulants were associated with slowing of overall growth of the cortical mantle.
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http://dx.doi.org/10.1176/appi.ajp.2008.08050781 | DOI Listing |
Background: White matter hyperintensities (WMH) were reported to contribute to the thinning of regional cortex connected to WMH in cerebral small vessel disease. However, the relationship between WMH and regional changes in WMH‐connected cortex in Alzheimer’s disease (AD) remains unclear. The objective of this study is to investigate the association between WMH and regional cortical thickness, amyloid and tau deposition, and synaptic density changes in the WMH‐connected cortex.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Division of Clinical Geriatrics, Center for Alzheimer Research, Department of Neurobiology, Care Sciences and Society, Karolinska Institutet, Stockholm, Sweden
Background: Although β‐amyloid and tau PET positivity (A+T+) has been related to neurodegeneration and cognitive decline in Alzheimer’s disease (AD), the driving force of neurodegeneration in discordant AT cases remains controversial. We investigated the impact of AT status on longitudinal rates of cortical atrophy and cognitive decline.
Method: A subset of 349 individuals (cognitively unimpaired [CU; n=230], cognitively impaired [CI; n=119]) with β‐amyloid and tau PET (a priori baseline), longitudinal MRI (interval; Mean=4.
Background: The structural brain alterations for subjective cognitive decline (SCD) and mild cognitive impairment (MCI) are poorly defined. We sought to characterize grey matter volume (GMV) and cortical thickness associated with SCD and MCI among rural‐dwelling older adults in China.
Method: This population‐based cross‐sectional study included 1072 dementia‐free participants derived from the brain MRI substudy of MIND‐China in 2018‐2020.
Alzheimers Dement
December 2024
Washington University in St. Louis, Saint Louis, MO, USA
Background: Alzheimer disease (AD) is a chronic progressive neurodegenerative disorder that presents with cognitive dysfunction, memory loss, language difficulties, emotion dysregulation, and the eventual loss of motor function and death. Magnetic resonance imaging (MRI) shows early atrophy in the medial temporal lobes, which then spreads to the posterior temporal lobe, parietal lobe, and finally the frontal lobe with relative sparing of the sensorimotor cortex. Social disadvantage has been shown to have potentially additive impacts on aging trajectories.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Amsterdam UMC, Amsterdam, Netherlands
Background: Different patterns of atrophy exist in the dementia stage of AD. However, little is known about the heterogeneity of atrophy patterns and the mechanisms that drive subsequent propagation of the disease in the preclinical stages.
Method: From the AMYPAD‐PNHS cohort, we included a total of 1323 non‐demented individuals, including 1094 amyloid‐negative, and 229 amyloid‐positive participants (Table 1).
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