Beyond words: an investigation of fine motor skills and the verbal communication spectrum in autism.

Introduction: This study investigated the associations between fine motor skills and expressive verbal abilities in a group of 97 autistic participants (age 8-17, mean=12.41) and 46 typically developing youth (age 8-17, mean=12.48). Methods: Participants completed assessments of motor and verbal communication skills, including finger tapping speed, grooved pegboard, grip strength, visual-motor integration tasks, and measures of speech and communication skills. ASD group performance on motor tests was compared to controls. Non-parametric tests were used to analyze group differences and correlations between motor and verbal communication skills. Based on prior research, we hypothesized that individuals on the autism spectrum would exhibit deficits in fine motor speed, dexterity, pencil motor control, but not manual motor strength. Additionally, we expected that impaired fine motor skills would be linked to poorer performance on standardized measures of verbal abilities. Results: The results indicated that 80% of autistic participants demonstrated an impairment on at least one measure of motor skills, and as a group, they exhibited significantly poorer fine motor performance compared to the non-ASD group in dominant hand finger tapping speed, bilateral fine motor dexterity measured via the grooved pegboard task, and pencil motor coordination and visual-motor integration measured on the Beery-Buktenica Developmental Test of Visual-Motor Integration-Sixth Edition. Moreover, impaired fine motor skills were associated with poorer performance on standardized clinical measures of verbal abilities, including articulation errors, receptive and expressive language and vocabulary, rapid naming, oromotor sequencing, and parent reported functional communication skills and social communication symptoms. Discussion: Overall,our findings suggest there is a high prevalence of fine motor impairments in ASD, and these impairments were associated with a range of verbal abilities. Further research is warranted to better understand the underlying mechanisms of these associations and develop targeted interventions to address both fine motor and verbal impairments in ASD.

Principal component analysis of synaptic density measured with [11C]UCB-J PET in early Alzheimer's disease.

BACKGROUND: Synaptic loss is considered an early pathological event and major structural correlate of cognitive impairment in Alzheimer's disease (AD). We used principal component analysis (PCA) to identify regional patterns of covariance in synaptic density using [11C]UCB-J PET and assessed the association between principal components (PC) subject scores with cognitive performance. METHODS: [11C]UCB-J binding was measured in 45 amyloid + participants with AD and 19 amyloid- cognitively normal participants aged 55-85. A validated neuropsychological battery assessed performance across five cognitive domains. PCA was applied to the pooled sample using distribution volume ratios (DVR) standardized (z-scored) by region from 42 bilateral regions of interest (ROI). RESULTS: Parallel analysis determined three significant PCs explaining 70.2% of the total variance. PC1 was characterized by positive loadings with similar contributions across the majority of ROIs. PC2 was characterized by positive and negative loadings with strongest contributions from subcortical and parietooccipital cortical regions, respectively, while PC3 was characterized by positive and negative loadings with strongest contributions from rostral and caudal cortical regions, respectively. Within the AD group, PC1 subject scores were positively correlated with performance across all cognitive domains (Pearson r = 0.24-0.40, P = 0.06-0.006), PC2 subject scores were inversely correlated with age (Pearson r = -0.45, P = 0.002) and PC3 subject scores were significantly correlated with CDR-sb (Pearson r = 0.46, P = 0.04). No significant correlations were observed between cognitive performance and PC subject scores in CN participants. CONCLUSIONS: This data-driven approach defined specific spatial patterns of synaptic density correlated with unique participant characteristics within the AD group. Our findings reinforce synaptic density as a robust biomarker of disease presence and severity in the early stages of AD.

Association of entorhinal cortical tau deposition and hippocampal synaptic density in older individuals with normal cognition and early Alzheimer's disease.

Sites of early neuropathologic change provide important clues regarding the initial clinical features of Alzheimer's disease (AD). We have shown significant reductions in hippocampal synaptic density in participants with AD, consistent with the early degeneration of entorhinal cortical (ERC) cells that project to hippocampus via the perforant path. In this study, [11C]UCB-J binding to synaptic vesicle glycoprotein 2A (SV2A) and [18F]flortaucipir binding to tau were measured via PET in 10 participants with AD (5 mild cognitive impairment, 5 mild dementia) and 10 cognitively normal participants. In the overall sample, ERC tau was inversely associated with hippocampal synaptic density (r = -0.59, p = 0.009). After correction for partial volume effects, the association of ERC tau with hippocampal synaptic density was stronger in the overall sample (r = -0.61, p = 0.007) and in the AD group where the effect size was large, but not statistically significant (r = -0.58, p = 0.06). This inverse association of ERC tau and hippocampal synaptic density may reflect synaptic failure due to tau pathology in ERC neurons projecting to the hippocampus.