Age-related macular degeneration (AMD) is a leading cause of visual dysfunction worldwide. Amyloid β (Aβ) peptides, Aβ1-40 (Aβ40) and Aβ1-42 (Aβ42), have been implicated previously in the AMD disease process. Consistent with a pathogenic role for Aβ, we show here that a mouse model of AMD that invokes multiple factors that are known to modify AMD risk (aged human apolipoprotein E 4 targeted replacement mice on a high-fat, cholesterolenriched diet) presents with Aβ-containing deposits basal to the retinal pigmented epithelium (RPE), histopathologic changes in the RPE, and a deficit in scotopic electroretinographic response, which is reflective of impaired visual function. Strikingly, these electroretinographic deficits are abrogated in a dose-dependent manner by systemic administration of an antibody targeting the C termini of Aβ40 and Aβ42. Concomitant reduction in the levels of Aβ and activated complement components in sub-RPE deposits and structural preservation of the RPE are associated with anti-Aβ40/42 antibody immunotherapy and visual protection. These observations are consistent with the reduction in amyloid plaques and improvement of cognitive function in mouse models of Alzheimer's disease treated with anti-Aβ antibodies. They also implicate Aβ in the pathogenesis of AMD and identify Aβ as a viable therapeutic target for its treatment.A ge-related macular degeneration (AMD) affects about 30% of Americans over 70 y of age (1-3) and is the leading cause of irreversible blindness in the Western world (4). It is a progressive retinal degenerative disease influenced by both environmental and genetic factors. Although the presence of a few small hard drusen is a normal, nonvision-impairing part of aging, the deposition of large diffuse drusen in the macula adversely impacts vision and is indicative of early AMD. As AMD progresses to late-stage disease, it is categorized as either dry [geographic atrophy with photoreceptor loss and extensive atrophy of the retinal pigmented epithelium (RPE)] or wet [exudative with subsequent choroidal neovascularization (CNV)] (5). Currently, there are no effective treatments for early AMD, and treatments for late-stage disease are limited to photodynamic therapy, macular translocation, and antivascular endothelial growth factor drugs (6-9).The strongest known risk factors are advanced age and cigarette smoking, with additional risk conferred by body mass index and diets high in fat (1,(10)(11)(12)(13)(14). The last decade has also yielded strong evidence that genotype, especially for genes involved in inflammation and the innate immune system, influences AMD risk and progression. Genes implicated as risk factors include complement factor H (CFH) (15-18), complement factor B (19), complement C3 (20), apolipoprotein E (APOE) (21-25), toll-like receptor 4 (26), LOC387715/ARMS2 (27, 28), HTRA1 (29, 30), ABCA4 (31), and fibulin 5 (32). Additional support for a role for chronic local inflammation in AMD comes from the discovery that protein components of drusen include activated co...

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A simple method of assessing 'index of disease activity' (IDA) in rheumatoid arthritis (RA) using a multivariate analysis (MVA) comprising morning stiffness (MS), pain scale (PS), grip strength (GS), articular index (AI), haemoglobin (Hb) and erythrocyte sedimentation rate (ESR) is described. The IDA of 99 patients with RA was assessed using MVA. The method could be used reliably and readily for random or longitudinal assessment, in drug trials and for comparing disease activity with other objective indices.

Traumatic brain injury (TBI) is a global cause of morbidity and mortality. Initial management and risk stratification of patients with TBI is made difficult by the relative insensitivity of screening radiographic studies as well as by the absence of a widely available, noninvasive diagnostic biomarker. In particular, a blood-based biomarker assay could provide a quick and minimally invasive process to stratify risk and guide early management strategies in patients with mild TBI (mTBI). Analysis of circulating exosomes allows the potential for rapid and specific identification of tissue injury. By applying acoustofluidic exosome separation—which uses a combination of microfluidics and acoustics to separate bioparticles based on differences in size and acoustic properties—we successfully isolated exosomes from plasma samples obtained from mice after TBI. Acoustofluidic isolation eliminated interference from other blood components, making it possible to detect exosomal biomarkers for TBI via flow cytometry. Flow cytometry analysis indicated that exosomal biomarkers for TBI increase in the first 24 h following head trauma, indicating the potential of using circulating exosomes for the rapid diagnosis of TBI. Elevated levels of TBI biomarkers were only detected in the samples separated via acoustofluidics; no changes were observed in the analysis of the raw plasma sample. This finding demonstrated the necessity of sample purification prior to exosomal biomarker analysis. Since acoustofluidic exosome separation can easily be integrated with downstream analysis methods, it shows great potential for improving early diagnosis and treatment decisions associated with TBI.