Social isolation is linked to classical risk factors of Alzheimer's disease-related dementias.

Alzheimer's disease and related dementias is a major public health burden-compounding over upcoming years due to longevity. Recently, clinical evidence hinted at the experience of social isolation in expediting dementia onset. In 502,506 UK Biobank participants and 30,097 participants from the Canadian Longitudinal Study of Aging, we revisited traditional risk factors for developing dementia in the context of loneliness and lacking social support. Across these measures of subjective and objective social deprivation, we have identified strong links between individuals' social capital and various indicators of Alzheimer's disease and related dementias risk, which replicated across both population cohorts. The quality and quantity of daily social encounters had deep connections with key aetiopathological factors, which represent 1) personal habits and lifestyle factors, 2) physical health, 3) mental health, and 4) societal and external factors. Our population-scale assessment suggest that social lifestyle determinants are linked to most neurodegeneration risk factors, highlighting them as promising targets for preventive clinical action.

Episodic memory in mild cognitive impairment inversely correlates with the global modularity of the cerebral blood flow network.

Cerebral blood flow (CBF) SPECT is an interesting methodology to study brain connectivity in mild cognitive impairment (MCI) since it is accessible worldwide and can be used as a biomarker of neuronal injury in MCI. In CBF SPECT, connectivity is grounded in group-based correlation networks. Therefore, topological metrics derived from the CBF correlation network cannot be used to support diagnosis and prognosis individually. However, methods to extract the individual patient contribution to topological metrics of group-based correlation networks were developed although not yet applied to MCI patients. Here, we investigate whether the episodic memory of 24 amnestic MCI patients correlates with individual patient contributions to topological metrics of the CBF correlation network. We first compared topological metrics of the MCI group network with the network corresponding to 26 controls. Metrics that showed significant differences were then used for the individual patient contribution analysis. We found that the global network modularity was increased while global efficiency decreased in the MCI network compared to the control. Most importantly, we found that episodic memory inversely correlates with the patient contribution to the global network modularity, which highlights the potential of this approach to develop a CBF connectivity-based biomarker at the individual level.

Diffusion tensor tractography reveals disrupted structural connectivity in childhood absence epilepsy.

PURPOSE: The structural connection patterns of the human brain are the underlying bases for functional connectivity. Although abnormal functional connectivity has been uncovered in childhood absence epilepsy (CAE) in previous electroencephalography and functional magnetic resonance imaging studies, little is known regarding the structural connectivity in CAE. We hypothesized that the structural connectivity would be disrupted in response to the decreased brain function in CAE. METHODS: Diffusion tensor imaging tractography was utilized to map the white matter (WM) structural network, composed of 90 cortical and sub-cortical regions, in 18 CAE and 18 age- and gender-matched healthy controls. Graph theoretical methods were applied to investigate the alterations in the topological and nodal properties of the networks in these patients. RESULTS: Both the CAE and the controls showed small-world properties in their WM networks. However, the network connection strength, absolute clustering coefficient, and global/local efficiency were significantly decreased, but characteristic path length was significantly increased in the CAE compared with the controls. Significantly decreased WM connections, nodal properties, and impaired sub-networks were found in the sub-cortical structures, orbitofrontal area, and limbic cortex in the CAE. Moreover, network connection strength, local efficiency, and nodal features in some regions were significantly negatively correlated with the duration of epilepsy. CONCLUSIONS: The present study demonstrated, for the first time, the disrupted topological organization of WM networks in CAE. The decreased connectivity and efficiency in the orbitofrontal and sub-cortical regions may serve as anatomical evidence to support the functional abnormalities related to the epileptic discharges observed in CAE. Moreover, the orbitofrontal sub-network may play a key role in CAE. These findings open up new avenues toward the understanding of absence epilepsy.