While ≧10,000 Americans turn 65 years old every day, only 10% of American homes are “aging ready.” Unsafe homes can exacerbate disability, lead to falls, and increase the likelihood of hospitalization. With increased investments in home and community-based services, public health stakeholders are considering home modifications to promote successful aging. While several home modification models exist, there is significant heterogeneity between models and no consensus on critical features. PubMed, EMBASE, and Web of Science were reviewed and twelve randomized controlled trials of home modifications for older adults were identified and evaluated for model structure, reported outcomes, and risk of bias. Overall, occupational therapist-driven home modifications supplemented with clinical, physical activity, and/or behavioral components saw the greatest success. This systematic review discusses the components of these models, highlights particularly effective and frequently used features, and the practice and research needed to create effective next-generation home modification models which promote healthy longevity.

Despite recent advancements in the field of neuro-ophthalmology, the rising rates of neurological and ophthalmological conditions, mismatches between supply and demand of clinicians, and an aging population underscore the urgent need to explore new therapeutic approaches within the field. Glucagon-like peptide 1 receptor agonists (GLP-1RAs), traditionally used in the treatment of type 2 diabetes, are becoming increasingly appreciated for their diverse applications. Recently, GLP-1RAs have been approved for the treatment of obesity and recognized for their cardioprotective effects. Emerging evidence indicates some GLP-1RAs can cross the blood-brain barrier and may have neuroprotective effects. Therefore, this article aims to review the literature on the neurologic and neuro-ophthalmic role of glucagon-like peptide 1 (GLP-1). This article describes GLP-1 peptide characteristics and the mechanisms mediating its known role in increasing insulin, decreasing glucagon, delaying gastric emptying, and promoting satiety. This article identifies the sources and targets of GLP-1 in the brain and review the mechanisms which mediate its neuroprotective effects, as well as implications for Alzheimer’s disease (AD) and Parkinson’s disease (PD). Furthermore, the preclinical works which unravel the effects of GLP-1 in ocular dynamics and the preclinical literature regarding GLP-1RA use in the management of several neuro-ophthalmic conditions, including diabetic retinopathy (DR), glaucoma, and idiopathic intracranial hypertension (IIH) are discussed.

In contrast to low-density lipoproteins which are atherogenic, high-density lipoproteins (HDL) have been conceptualized as beneficial modulators of adverse pathophysiological phenomena along arterial walls. The HDLs are characterized by highly complex and varied molecular cargoes that include apoproteins, enzymes, microRNAs, bioactive lipids and phospholipids, components of complement, and immune factors, among others. These cargo components determine its functionality. Despite the findings of Mendelian inheritance studies which suggest that HDL is not causal in the pathway for atherogenesis, experiments with HDLs show that it can drive reverse cholesterol transport and antagonize inflammation, oxidation, thrombosis, platelet aggregation, endothelial progenitor cell mobilization, potentiate immunity, foster communication between different cell and tissue types, and function as a crucial apoprotein donor amongst the various lipoproteins. These functions are understandably viewed as beneficial and antagonize pathophysiology. Secondary to the complexity of its proteome and lipidome, HDL functionality is profoundly responsive to the metabolic and genetic backgrounds of individuals. Even its size and lipidation status can influence its functionality. As part of the acute phase response, critical antioxidative moieties can be replaced by such acute phase reactants as serum amyloid A and pro-oxidative enzymes. The functionality of HDL is influenced by chronic kidney disease, coronary artery disease, acute myocardial infarction, obesity, insulin resistance, metabolic syndrome, diabetes mellitus, and cancer. Herein we describe many of the alterations in HDL constitution and the resulting changes in functional capacity that can be observed. A unifying theme characterizing these disease states is that they all heighten systemic inflammatory tone and potentiate a pro-oxidative state. These changes clearly associate with profound changes in the functionality and behavior of HDL particles. We are only beginning to comprehend the extraordinary complexity and range of biochemical functions, both beneficial and injurious, that this lipoprotein can regulate. Hence it was extremely premature to think that simply raising HDL cholesterol in serum would beneficially influence cardiovascular morbidity and mortality. We have a long way to go before we develop a more comprehensive and potentially therapeutically relevant understanding of how to better harness its potential for antagonizing disease and block its ability to participate in and adversely influence the course of disease.

Gene therapy offers a promising new frontier in the treatment of inherited and acquired retinal disease. This review describes the current surgical delivery approaches for gene therapy to the retina—subretinal, suprachoroidal, and intravitreal—and provides an update on the state of the art for each method in 2025.

Lysosomal acid lipase deficiency (LAL-D) is underrecognized because it manifests clinically with lipid and lipoprotein values similar to those observed in heterozygous familial hypercholesterolemia (FH). Although LAL-D is uncommon, understanding the differences between the 2 diseases has significant management implications. We present a case of LAL-D that masqueraded as FH. (Level of Difficulty: Advanced.)