Eye: In Parkinson's Disease & Alzheimerâ€™s Disease
There are increasing lines of evidence showing that neurodegeneration in Alzheimer’s disease (AD) and Parkinson’s disease (PD) is not limited to the brain but also occurs in the retina. Consequently, AD/PD patients can gradually develop vision problems. This neurological and ophthalmological disorder creates a pressing need for developing therapy to treat vision impairment in AD/PD. On the other hand, pathophysiological changes in the retina may reflect what might happen in the same diseases in the brain. Thus retinal studies may allow us to develop quantifiable measures for the diagnosis and prognosis of disease progression. Furthermore, parallel or early pathophysiological changes of the retina in AD/PD allow us to study retina-brain interactions.
Several research groups have made advances in understanding pathophysiological changes of the retina in the eyes in AD/PD. It is the time to re-evaluate this issue. The aim of this Research Topic is to make collective effort to review the progress in this newly emerging multi-disciplinary field, to stimulate more research in AD/PD and Ophthalmology communities. The aim of this Research Topic is not simply to review, but also to foster cross-fertilization among neurobiologists, ophthalmologists, optometrist, neurologists and psychologist investigating vision cognition toward developing translational neuroscience of the retina in neurodegenerative diseases of the brain.
We also cover studies which point beyond current theories of neurodegeneration in PD & AD. The range of articles will encompass basic retina information on dopaminergic mechanisms, alpha-synuclein and tau pathology in the brain. Alpha-synuclein is a misfolded protein. Its aggregation as Lewy body is pathological hallmark of PD. However, retinal pathology in PD is not confined to dopaminergic neurons in PD. It could affect synaptic connections in the retinal ganglion cells and inner nuclear layers. This kind of pathological changes could also be found in the AD retina. Research has suggested capillary remodeling in PD, AD and in Leber’s Hereditary Optic Neuropathy (LHON). There is evidence of regulation of endothelial function by reactive oxygen species, and we wish to consider studies addressing the role of mitochondrial dysfunction, endothelium and growth factors. For AD, increasing lines of evidence have shown that ß-amyloid peptide and tau pathology can be found in the retina and optic nerve, which impair axonal transport and synaptic connections between different layers of the retina. It has been reported that disease progression in AD can be reflected by the thickness of the retina. Studies on neuroprotective therapies at the retinal level with potentials for generalizations for process in the brain in AD/PD are also welcome.
Journal of Clinical and Experimental Ophthalmology
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