Blue light-induced retinal damage: A brief review and a proposal for examining the hypothetical causal link between person digital device use and retinal injury

Background: There is growing concern that the increased use of personal digital devices, which emit a high proportion of their light in the blue wavelengths, may have harmful effects on the retina. Extensive historical as well as current research demonstrates that exposure to high energy visible light (blue light) can damage the retina under certain circumstances. There are, however, no studies that directly address whether blue light at the intensities emitted by digital devices can potentially cause such harm. The present review aimed to examine whether blue light exposure from computers, tablets, and cell phones can, when used habitually over a prolonged period of time, be harmful to the retinal. Methods: A search of the literature on blue light-induced retinal damage was performed using a number of scientific search engines, including BioOne Completeâ„¢, Google Scholarâ„¢, Paperityâ„¢, PubMedâ„¢, and ScienceOpenâ„¢. Studies most significant for addressing the question of possible harmful effects of blue light emitted by personal digital devices were selected from this search and reviewed. Results: The data from the selected studies were summarized and their limitations in addressing the question of whether the blue light from personal digital devices is capable of producing retinal damage were addressed. Based on these limitations, a practical experimental protocol for collecting the additional data needed was proposed. Data from pilot experiments are presented that indicate the practicality of this approach. Conclusions: The currently available data on the effects of blue light on the retina are not sufficient to refute the hypothesis that the use of personal digital devices could, over a lifetime, produce retinal damage. Additional studies, such as those proposed in this article, are needed to resolve this issue

An update on RPE cell senescence as a key contributor to age-related macular degeneration: support from current and experimental treatments

Background: Age-related macular degeneration (AMD) is a major cause of vision loss. Its prevalence has increased over the past decade. This increase is partly due to the scarcity of preventive and therapeutic interventions for this disorder, except when it is in its advanced neovascular form. Discovery of effective treatments for AMD is complicated by the multifactorial pathology of the disorder. Thus, it is difficult to determine which potential disease mechanism to target in order to achieve the greatest clinical benefit. Hypothesis: Over a decade ago, it was hypothesized that many of the pathologies observed in AMD stem from retinal pigment epithelial (RPE) cell senescence. This provided a potentially key mechanistic target. Supporting this hypothesis, many of the agents that were in development or clinical use for AMD at that time influenced RPE cell senescence, although they were not utilized for this specific effect. The present article re-evaluates this hypothesis by exploring the logical prediction that if RPE cell senescence is a key contributor to AMD, then inhibition of RPE cell senescence is important in the treatment of AMD. If this hypothesis holds true, the inhibition or reversal of RPE cell senescence or its effects should be a common characteristic of new treatments for AMD. Conclusions: Over the past decade, many agents have been investigated for the treatment of AMD. Although a few were designed to address cell senescence, the majority targeted other potential pathological mechanisms. In support of our original hypothesis, we now present evidence that many of the newer agents investigated for the treatment of AMD, even those that were not meant to reduce cell senescence or its effects, have this function as part of their activity profiles. Further experimental studies or clinical trials exploring the safety and efficacy of inhibiting RPE cell senescence or reversing its effects are needed to pave the way for improved AMD treatment

Association of metformin use with age-related macular degeneration risk

Background: The association between metformin use and reduced age-related macular degeneration (AMD) risk has been explored. Studies have shown a positive association, no association, or ambiguous results. The aim of this narrative review is to compile these divergent findings, and thereby, better assess the potential of metformin use in reducing the AMD risk. Methods: Studies were extracted in two ways. First, a standard Google Scholar™ search was performed using the keywords “metformin” AND “macular degeneration” without language or time restrictions. The full texts of relevant articles identified in this search were retrieved and assessed, and articles of peer-reviewed original studies and meta-analyses were included. Second, the reference lists of the included articles were used to identify additional articles that satisfied the search algorithm and included in this review. Results: Of the 12 studies included in this review, eight showed a positive correlation between metformin use and a reduced AMD risk, while one showed no association. Of the eight positive studies, seven were retrospective. Apart from the design, the studies were also diverse. The number of participants in each study ranged from over 300 to 30 million person-years. The study populations included those with type 2 diabetes mellitus, those with AMD, and those without either. The study locations were the United States, Europe, and Asia. The ambiguous or negative results from four studies could largely be rationalized based on the confounding factor of study design. Conclusions: Most studies examined in this review demonstrated a positive association between metformin use and a reduced AMD risk. Studies not reporting such an association did not definitively demonstrate its absence. Overall, the studies reviewed herein support further clinical investigation of metformin as a prophylactic and potential treatment modality for AMD. Further randomized clinical trials with reasonably longer follow-up periods are necessary to determine the generalizability of the findings of studies reporting positive results

Monoclonal Antibody Identification of Subpopulations of Cerebral Cortical Neurons Affected in Alzheimer disease

Neuronal degeneration is one of the hallmarks of Alzheimer disease (AD). Given the paucity of molecular markers available for the identification of neuronal subtypes, the specificity of neuronal loss within the cerebral cortex has been difficult to evaluate. With a panel of four monoclonal antibodies (mAbs) applied to central nervous system tissues from AD patients, we have immunocytochemically identified a population of vulnerable cortical neurons; a subpopulation of pyramidal neurons is recognized by mAbs 3F12 and 44.1 in the hippocampus and neocortex, and clusters of multipolar neurons in the entorhinal cortex reactive with mAb 44.1 show selective degeneration. Closely adjacent stellate-like neurons in these regions, identified by mAb 6A2, show striking preservation in AD. The neurons recognized by mAbs 3F12 and 44.1, to the best of our knowledge, do not comprise a single known neurotransmitter system. mAb 3A4 identifies a phosphorylated antigen that is undetectable in normal brain but accumulates early in the course of AD in somas of vulnerable neurons. Antigen 3A4 is distinct from material reactive with thioflavin S or antibody generated against paired helical filaments. Initially, antigen 3A4 is localized to neurons in the entorhinal cortex and subiculum, later in the association neocortex, and, ultimately in cases of long duration, in primary sensory cortical regions. mAb 3F12 recognizes multiple bands on immunoblots of homogenates of normal and Ad cortical tissues, whereas mAb 3A4 does not bind to immunoblots containing neurofilament proteins or brain homogenates from AD patients. Ultrastructurally, antigen 3A4 is localized to paired-helical filaments. Using these mAbs, further molecular characterization of the affected cortical neurons is now possible

Request and Augment Presentation

The Request and Augment steps to curating research data are explained in this presentation