Innate immune biology in age-related macular degeneration.

Age-related macular degeneration (AMD) is a neurodegenerative disease and a leading cause of irreversible vision loss in the developed world. While not classically described as an inflammatory disease, a growing body of evidence has implicated several components of the innate immune system in the pathophysiology of age-related macular degeneration. In particular, complement activation, microglial involvement, and blood-retinal-barrier disruption have been shown to play key roles in disease progression, and subsequent vision loss. This review discusses the role of the innate immune system in age-related macular degeneration as well as recent developments in single-cell transcriptomics that help advance the understanding and treatment of age-related macular degeneration. We also explore the several potential therapeutic targets for age-related macular degeneration in the context of innate immune activation.

In Context: A Developmental Model of Reward Processing, With Implications for Autism and Sensitive Periods.

OBJECTIVE: Differences in reward processing have been associated with numerous psychiatric disorders, including autism and attention-deficit/hyperactivity disorder (ADHD). Many attempts to understand reward processing characterize differences in clinical populations after disorder onset; however, divergence may begin much earlier. In fact, the typical developmental progression of reward processing in infancy and early childhood is poorly understood. We re-conceptualize classic infant developmental constructs such as preferential looking into a Six-Component Developmental Model of Reward Processing: an infant- and young child-focused framework to guide research and assessment of reward processing across development. METHOD: The extant developmental literature including recent textbooks, systematic reviews, and meta-analyses was reviewed to build a conceptual framework. We describe experimental paradigms to assess each developmental component of reward processing longitudinally from infancy. A timeline of each component's emergence was estimated. RESULTS: Six components of reward processing were identified-association, discrimination, preference/valuation, effort, anticipation, and response. Selected evidence suggests emergence between birth and 6 months. Application of this model to autism led to a reinterpretation of existing disparate results, and illuminated a path to study the developmental processes underlying a popular hypothesis of autism, the motivation hypothesis. Current evidence further suggests that a sensitive period may exist for the emergence of reward processing. CONCLUSION: The proposed framework offers a useful reconceptualization of the extant literature. Future longitudinal work using the suggested experimental paradigms with high-risk populations could elucidate the developmental trajectory of the components and timing of potential sensitive period(s) for each component.