Intramodal cortical plastic changes after moderate visual impairment in human amblyopia.

Early blindness results in alterations in the neural responses to auditory stimuli. Here we show that even moderately reduced vision in one eye early in life is sufficient to induce neural plastic changes in voice processing. We asked individuals with reduced visual acuity in one eye due to amblyopia to attend to vocal cues during electroencephalogram recording. We found enhanced frontal auditory responses at 125 ms-225 ms, which were correlated with reduced vision in the amblyopic eye, but not the fellow eye. Our results indicate intramodal reorganization, typically observed after congenital profound visual deprivation.

Neural correlates of visual spatial selective attention are altered at early and late processing stages in human amblyopia.

Amblyopia is a neurodevelopmental visual disorder which results in reduced visual acuity in one eye and impaired binocular interactions. Previous studies suggest attentional deficits in amblyopic individuals. However, spatial cues which orient attention to a visual field improved performance. Here, we investigate the neural correlates of auditory-visual spatial selective attention in amblyopia during EEG recording. An auditory cue, that was followed by the presentation of two Gabor patches presented in the lower left and right visual fields, indicated the most likely location of an upcoming target Gabor. The target Gabor differed in orientation from the more frequently presented non-target Gabor patches. Adults with amblyopia and neurotypical observers were asked to detect the target Gabor monocularly at the cued location, while withholding their response to targets presented at the uncued location and to all non-target Gabor patches. Higher response rates were observed for cued compared to uncued targets in both groups. However, amblyopic individuals detected targets less efficiently with their amblyopic eye as compared to their fellow eye. Correspondingly, event-related potentials (ERPs) recorded to the onset of the non-target Gabor patches were delayed at early processing stages (150-300 ms: posterior N100) and reduced in amplitude at later time windows (150-350 ms: P200, 300-500 ms: sustained activity) in the amblyopic eye compared to the fellow eye. Such interocular differences were not observed in neurotypical observers. These findings suggest that neural resources allocated to the early formation of visual discrimination as well as later stimulus recognition processes are altered in the amblyopic eye.

TGF-ß Signaling: A Therapeutic Target to Reinstate Regenerative Plasticity in Vascular Dementia?

Vascular dementia (VaD) is the second leading form of memory loss after Alzheimer's disease (AD). Currently, there is no cure available. The etiology, pathophysiology and clinical manifestations of VaD are extremely heterogeneous, but the impaired cerebral blood flow (CBF) represents a common denominator of VaD. The latter might be the result of atherosclerosis, amyloid angiopathy, microbleeding and micro-strokes, together causing blood-brain barrier (BBB) dysfunction and vessel leakage, collectively originating from the consequence of hypertension, one of the main risk factors for VaD. At the histopathological level, VaD displays abnormal vascular remodeling, endothelial cell death, string vessel formation, pericyte responses, fibrosis, astrogliosis, sclerosis, microglia activation, neuroinflammation, demyelination, white matter lesions, deprivation of synapses and neuronal loss. The transforming growth factor (TGF) ß has been identified as one of the key molecular factors involved in the aforementioned various pathological aspects. Thus, targeting TGF-ß signaling in the brain might be a promising therapeutic strategy to mitigate vascular pathology and improve cognitive functions in patients with VaD. This review revisits the recent understanding of the role of TGF-ß in VaD and associated pathological hallmarks. It further explores the potential to modulate certain aspects of VaD pathology by targeting TGF-ß signaling.