Topic: retinal degeneration

Understanding the retina in health and disease is a key issue for neuroscience and neuroengineering applications such as retinal prostheses. Although the processing of visual information in the healthy retina has been studied in detail, no comprehensive computational model exists that captures the many cell-level and network-level biophysical changes common to retinal degenerative diseases. To address this challenge, we developed a biophysically detailed model of the retinal circuitry and simulated the network-level response to both light and electrical stimulation. The model included 11,138 c

Understanding the retina in health and disease is a key issue for neuroscience and neuroengineering applications such as retinal prostheses. Although the processing of visual information in the healthy retina has been studied in detail, no comprehensive computational model exists that captures the many cell-level and network-level biophysical changes common to retinal degenerative diseases. To address this challenge, we developed a biophysically detailed model of the retinal circuitry and simulated the network-level response to both light and electrical stimulation. The model included 11,138 c

By applying electrical stimulation, retinal prostheses aim to bypass dysfunctional photoreceptors and directly activate retinal ganglion cells (RGCs). Therefore, effective modulation of RGCs is the key step in the development of retinal prostheses. Six cynomolgus monkeys were used: three as a control and the other three as an N-methyl-N-nitrosourea (MNU)-induced retinal degeneration model. The retinal recording was performed using the 8x8 multi-electrode array. Figure shows the electrical stimulation pulses (a), raster plots of RGC spikes (b), and the modulation efficiency score (MES) (c). The

The aberrant formation and accumulation of the misfolded polyglutamine （polyQ） containing proteins in the nuclei are considered to be the major hallmark and cause of many neurodegenerative diseases, including Spinocerebellar ataxias （SCAs）, Huntington Disease （HD）, Spinal and Bulbar Muscular Atrophy （SBMA）, and Dentatorubro pallidoluysian atrophy （DRPLA）. It is, therefore, believed that intervening biosynthesis, resolution, and clearance of the misfolded proteins, may represent potential therapeutic approaches. Previous studies have found that the BFRF1 protein of the Epstein-Barr virus （EBV）

Most forms of induced and inherited retinal degeneration involve induction of neuroinflammation that is characterized by changes in Müller glia and microglia, and at least some of these changes accelerate vision loss in advanced blinding diseases. The specific triggers, hierarchy of molecular steps, and cellular interactions that promote these changes initially are still largely obscure. However, it is generally thought that Müller glia and microglia activation is secondary to distress signals and cellular debris following programmed cell death of photoreceptor or other neurons in the retina.

Electrical-based neuroprostheses reported promising clinical outcomes for the treatment of neurological disorders. Nevertheless, they suffer from low spatial resolution and lack of natural neurotransmission specificity that require alternative bio-mimetic stimulation strategies. Chemical-based neuroprostheses would represent a promising option to emulate the physiological synaptic communication by providing localized delivery of neurotransmitters. While various drug delivery approaches have been investigated, an efficient neurotransmitter-based neuronal stimulation at the nanoscale still remai