Effects of change in FreeSurfer version on classification accuracy of patients with Alzheimer's disease and mild cognitive impairment.

Studies have found non-negligible differences in cortical thickness estimates across versions of software that are used for processing and quantifying MRI-based cortical measurements, and issues have arisen regarding these differences, as obtained estimates could potentially affect the validity of the results. However, more critical for diagnostic classification than absolute thickness estimates across versions is the inter-subject stability. We aimed to investigate the effect of change in software version on classification of older persons in groups of healthy, mild cognitive impairment and Alzheimer's Disease. Using MRI samples of 100 older normal controls, 100 with mild cognitive impairment and 100 Alzheimer's Disease patients obtained from the Alzheimer's Disease Neuroimaging Initiative database, we performed a standard reconstruction processing using the FreeSurfer image analysis suite versions 4.1.0, 4.5.0 and 5.1.0. Pair-wise comparisons of cortical thickness between FreeSurfer versions revealed significant differences, ranging from 1.6% (4.1.0 vs. 4.5.0) to 5.8% (4.1.0 vs. 5.1.0) across the cortical mantle. However, change of version had very little effect on detectable differences in cortical thickness between diagnostic groups, and there were little differences in accuracy between versions when using entorhinal thickness for diagnostic classification. This lead us to conclude that differences in absolute thickness estimates across software versions in this case did not imply lacking validity, that classification results appeared reliable across software versions, and that classification results obtained in studies using different FreeSurfer versions can be reliably compared. Hum Brain Mapp 37:1831-1841, 2016. © 2016 Wiley Periodicals, Inc.

Cortical thickness and surface area relate to specific symptoms in early relapsing-remitting multiple sclerosis.

BACKGROUND: Cortical atrophy is common in early relapsing-remitting multiple sclerosis (RRMS). Whether this atrophy is caused by changes in cortical thickness or cortical surface area is not known, nor is their separate contributions to clinical symptoms. OBJECTIVES: To investigate the difference in cortical surface area, thickness and volume between early RRMS patients and healthy controls; and the relationship between these measures and neurological disability, cognitive decline, fatigue and depression. METHODS: RRMS patients (n = 61) underwent magnetic resonance imaging (MRI), neurological and neuropsychological examinations. We estimated cortical surface area, thickness and volume and compared them with matched healthy controls (n = 61). We estimated the correlations between clinical symptoms and cortical measures within the patient group. RESULTS: We found no differences in cortical surface area, but widespread differences in cortical thickness and volume between the groups. Neurological disability was related to regionally smaller cortical thickness and volume. Better verbal memory was related to regionally larger surface area; and better visuo-spatial memory, to regionally larger cortical volume. Higher depression scores and fatigue were associated with regionally smaller cortical surface area and volume. CONCLUSIONS: We found that cortical thickness, but not cortical surface area, is affected in early RRMS. We identified specific structural correlates to the main clinical symptoms in early RRMS.

The subcellular distribution of T-type Ca2+ channels in interneurons of the lateral geniculate nucleus.

Inhibitory interneurons (INs) in the lateral geniculate nucleus (LGN) provide both axonal and dendritic GABA output to thalamocortical relay cells (TCs). Distal parts of the IN dendrites often enter into complex arrangements known as triadic synapses, where the IN dendrite plays a dual role as postsynaptic to retinal input and presynaptic to TC dendrites. Dendritic GABA release can be triggered by retinal input, in a highly localized process that is functionally isolated from the soma, but can also be triggered by somatically elicited Ca(2+)-spikes and possibly by backpropagating action potentials. Ca(2+)-spikes in INs are predominantly mediated by T-type Ca(2+)-channels (T-channels). Due to the complex nature of the dendritic signalling, the function of the IN is likely to depend critically on how T-channels are distributed over the somatodendritic membrane (T-distribution). To study the relationship between the T-distribution and several IN response properties, we here run a series of simulations where we vary the T-distribution in a multicompartmental IN model with a realistic morphology. We find that the somatic response to somatic current injection is facilitated by a high T-channel density in the soma-region. Conversely, a high T-channel density in the distal dendritic region is found to facilitate dendritic signalling in both the outward direction (increases the response in distal dendrites to somatic input) and the inward direction (the soma responds stronger to distal synaptic input). The real T-distribution is likely to reflect a compromise between several neural functions, involving somatic response patterns and dendritic signalling.