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Fluorodeoxyglucose positron emission tomography (FDG-PET) imaging based 3D topographic brain glucose metabolism patterns from normal controls (NC) and individuals with dementia of Alzheimer's type (DAT) are used to train a novel multi-scale ensemble classification model. This ensemble model outputs a FDG-PET DAT score (FPDS) between 0 and 1 denoting the probability of a subject to be clinically diagnosed with DAT based on their metabolism profile. A novel 7 group image stratification scheme is devised that groups images not only based on their associated clinical diagnosis but also on past and future trajectories of the clinical diagnoses, yielding a more continuous representation of the different stages of DAT spectrum that mimics a real-world clinical setting. The potential for using FPDS as a DAT biomarker was validated on a large number of FDG-PET images (N=2984) obtained from the Alzheimer's Disease Neuroimaging Initiative (ADNI) database taken across the proposed stratification, and a good classification AUC (area under the curve) of 0.78 was achieved in distinguishing between images belonging to subjects on a DAT trajectory and those images taken from subjects not progressing to a DAT diagnosis. Further, the FPDS biomarker achieved state-of-the-art performance on the mild cognitive impairment (MCI) to DAT conversion prediction task with an AUC of 0.81, 0.80, 0.77 for the 2, 3, 5 years to conversion windows respectively.
Childhood traumatic brain injury (TBI) is one of the most common causes of acquired disability and has significant implications for executive functions (EF), such as impaired attention, planning, and initiation that are predictive of everyday functioning. Evidence has suggested attentional features of executive functioning require behavioral flexibility that is dependent on frontostriatial circuitry. The purpose of this study was to evaluate surface-based deformation of a specific frontostriatial circuit in pediatric TBI and its role in EF. Regions of interest included: the dorsolateral prefrontal cortex (DLPFC), caudate nucleus, globus pallidus, and the mediodorsal nucleus of the thalamus (MD). T1-weighted magnetic resonance images were obtained in a sample of children ages 8-13 with complicated mild, moderate, or severe TBI (n = 32) and a group of comparison children with orthopedic injury (OI; n = 30). Brain regions were characterized using high-dimensional surface-based brain mapping procedures. Aspects of EF were assessed using select subtests from the Test of Everyday Attention for Children (TEA-Ch). General linear models tested group and hemisphere differences in DLPFC cortical thickness and subcortical shape of deep-brain regions; Pearson correlations tested relationships with EF. Main effects for group were found in both cortical thickness of the DLPFC (F1,60 = 4.30, p = 0.042) and MD mean deformation (F1,60 = 6.50, p = 0.01) all with lower values in the TBI group. Statistical surface maps revealed significant inward deformation on ventral-medial aspects of the caudate in TBI relative to OI, but null results in the globus pallidus. No significant relationships between EF and any region of interest were observed. Overall, findings revealed abnormalities in multiple aspects of a frontostriatial circuit in pediatric TBI, which may reflect broader pathophysiological mechanisms. Increased consideration for the role of deep-brain structures in pediatric TBI can aid in the clinical characterization of anticipated long-term developmental effects of these individuals.
Frontotemporal dementia (FTD) is a neurodegenerative disease with a strong genetic basis. Understanding the structural brain changes during pre-symptomatic stages may allow for earlier diagnosis of patients suffering from FTD; therefore, we investigated asymptomatic members of FTD families with mutations in C9orf72 and granulin (GRN) genes. Clinically asymptomatic subjects from families with C9orf72 mutation (15 mutation carriers, C9orf72+; and 23 non-carriers, C9orf72-) and GRN mutations (9 mutation carriers, GRN+; and 15 non-carriers, GRN-) underwent structural neuroimaging (MRI). Cortical thickness and subcortical gray matter volumes were calculated using FreeSurfer. Group differences were evaluated, correcting for age, sex and years to mean age of disease onset within the subject's family. Mean age of C9orf72+ and C9orf72- were 42.6 ± 11.3 and 49.7 ± 15.5 years, respectively; while GRN+ and GRN- groups were 50.1 ± 8.7 and 53.2 ± 11.2 years respectively. The C9orf72+ group exhibited cortical thinning in the temporal, parietal and frontal regions, as well as reduced volumes of bilateral thalamus and left caudate compared to the entire group of mutation non-carriers (NC: C9orf72- and GRN- combined). In contrast, the GRN+ group did not show any significant differences compared to NC. C9orf72 mutation carriers demonstrate a pattern of reduced gray matter on MRI prior to symptom onset compared to GRN mutation carriers. These findings suggest that the preclinical course of FTD differs depending on the genetic basis and that the choice of neuroimaging biomarkers for FTD may need to take into account the specific genes involved in causing the disease.
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