Microinfarcts are a common clinical feature of the aging brain, particularly in patients with cognitive decline, vascular or Alzheimer’s dementia. However, the natural history of these lesions remains largely unexplored. Here we describe a mouse (C57BL/6J) model of multiple diffuse microinfarcts induced by unilateral internal carotid artery injection of cholesterol crystals (40-70μm). Microinfarcts were spread throughout the deep cortex, subcortical tissue and hippocampus and were comprised of a CD68 (a marker for reactive microglia and macrophages)-positive core surrounded by large regions of GFAP-positive reactive astrogliosis. Widespread reactive gliosis, including mislocalization of the astrocytic water channel aquaporin-4 (AQP4) persisted long after injury, recovering only after 1 month post-stroke. Within the cortex, neuronal cell death progressed gradually over the first month, from ~35% at 3 days to 60% at 28 days post-stroke. Delayed demyelination was also observed in lesions, beginning 28 days post-stroke. These findings demonstrate that microinfarct development follows a distinct course compared to larger regional infarcts such as those induced by middle cerebral artery occlusion. The long-lasting gliosis, delayed neuronal loss and demyelination suggest that the therapeutic window for microinfarcts may be much wider (perhaps days to weeks) than for larger strokes.
A new technique for displacement measurement is proposed that makes use of phase singularities in the complex signal generated by a Laguerre-Gauss filter operation applied to a speckle pattern. The core structures of phase singularities are used as unique fingerprints attached to the object surface, and the displacement is determined by tracing the movement of registered phase singularities with their correspondence being identified by the fingerprints. Experimental results for translational and rotational displacement measurements are presented that demonstrate large dynamic range and high spatial resolution of the proposed optical vortex metrology.
Aims
Lifestyle interventions are an important and viable approach for preventing cognitive deficits. However, the results of studies on alcohol, coffee and tea consumption in relation to cognitive decline have been divergent, likely due to confounds from dose–response effects. This meta-analysis aimed to find the dose–response relationship between alcohol, coffee or tea consumption and cognitive deficits.
Methods
Prospective cohort studies or nested case-control studies in a cohort investigating the risk factors of cognitive deficits were searched in PubMed, Embase, the Cochrane and Web of Science up to 4th June 2020. Two authors searched the databases and extracted the data independently. We also assessed the quality of the studies with the Newcastle-Ottawa scale. Stata 15.0 software was used to perform model estimation and plot the linear or nonlinear dose–response relationship graphs.
Results
The search identified 29 prospective studies from America, Japan, China and some European countries. The dose–response relationships showed that compared to non-drinkers, low consumption (<11 g/day) of alcohol could reduce the risk of cognitive deficits or only dementias, but there was no significant effect of heavier drinking (>11 g/day). Low consumption of coffee reduced the risk of any cognitive deficit (<2.8 cups/day) or dementia (<2.3 cups/day). Green tea consumption was a significant protective factor for cognitive health (relative risk, 0.94; 95% confidence intervals, 0.92–0.97), with one cup of tea per day brings a 6% reduction in risk of cognitive deficits.
Conclusions
Light consumption of alcohol (<11 g/day) and coffee (<2.8 cups/day) was associated with reduced risk of cognitive deficits. Cognitive benefits of green tea consumption increased with the daily consumption.
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