Purpose To review the impact of increased digital device usage arising from lockdown measures instituted during the COVID-19 pandemic on myopia, and make recommendations for mitigating potential detrimental effects on myopia control. Design Perspective Methods Review of studies focused on digital device usage, near work, and outdoor time in relation to myopia onset and progression. Public health policies on myopia control, recommendations on screen time and information pertaining to the impact of COVID-19 on increased digital device use were presented. Recommendations to minimize the impact of the pandemic on myopia onset and progression in children were made. Results Increased digital screen time, near work and limited outdoor activities were found to be associated with the onset and progression of myopia, and could potentially be aggravated during and beyond the COVID-19 pandemic outbreak period. While school closures may be short-lived, increased access, adoption and dependence on digital devices could have a long term negative impact on childhood development. Raising awareness among parents, children and government agencies is key to mitigating myopigenic behaviours that may become entrenched during this period. Conclusions While it is important to adopt critical measures to slow or halt the spread of COVID-19, close collaboration between parents, schools and ministries is necessary to assess and mitigate the long term collateral impact of COVID-19 on myopia control policies.

Our aim was to determine changes in free amino acid (FAA) and dipeptide (DP) concentrations in probable Alzheimer's disease (pAD) subjects compared with control (CT) subjects using liquid chromatography and electrospray ionization tandem mass spectrometry (LCMS2). We recruited gender- and age-matched study participants based on neurological and neuropsychological assessments. We measured FAAs and DPs in cerebrospinal fluid (CSF), plasma and urine using LCMS2 with selected reaction monitoring (SRM). Imidazole-containing FAAs (histidine, methyl-histidine), catecholamines (L-DOPA and dopamine), citrulline, ornithine, glycine and antioxidant DPs (carnosine and anserine) accounted for the major changes between CT and pAD. Carnosine levels were significantly lower in pAD (328.4 +/- 91.31 nmol/dl) than in CT plasma (654.23 +/- 100.61 nmol/dl). In contrast, L-DOPA levels were higher in pAD (1400.84 +/- 253.68) than CT (513.10 +/- 121.61 nmol/dl) plasma. These data underscore the importance of FAA and DP metabolism in the pathogenesis of AD. Since our data show changes in antioxidants, neurotransmitters and their precursors, or FAA associated with urea metabolism in pAD compared with CT, we propose that manipulation of these metabolic pathways may be important in preventing AD progression.