There are currently more than 38.9 million people over the age of 65 in the United States. Up to 3.6 million of these people are considered housebound and in need of home-based care. Although homebound status is not defined specifically, with a broad range of disability levels, it is evident that people who are homebound suffer from a multitude of medical and psychiatric illnesses. This review examines the current literature to identify the specific physical and psychiatric factors most responsible for the elderly becoming and remaining housebound. The homebound elderly suffer from metabolic, cardiovascular, cerebrovascular, and musculoskeletal diseases, as well as from cognitive impairment, dementia and depression, at higher rates than the general elderly population. The information in this review will explain the specific types of care the homebound population need, and discuss the care that could help ease their suffering and delay their entry into a nursing home or hospital.

Background Amyloid-associated depression is associated with cognitive impairment cross sectionally. This follow-up study was to determine the relationship between amyloid-associated depression and the development of Alzheimer’s disease (AD). Methods Two hundred and twenty three subjects who did not have dementia at baseline were given a repeat cognitive evaluation for incident AD. Depression was defined by having a Center for Epidemiological Studies Depression (CES-D) score ≥ 16, and non-amyloid vs. amyloid-associated depression by having a low vs. high plasma amyloid-β peptide 40 (Aβ40)/Aβ42 ratio. Apolipoprotein E (ApoE) genotype was determined, and antidepressant usage was documented. Results Fifteen subjects developed AD (7%) after an average follow-up time of 6.2 years. While none of those with non-amyloid depression developed AD, 9% of those with amyloid-associated depression developed AD. Further, among those with amyloid-associated depression, ApoE4 carriers tended to have a higher risk of AD than ApoE4 non-carriers (40% vs. 4%, p=0.06). In contrast, 8% of those who did not have depression at baseline developed AD, but ApoE4 carriers and non-carriers did not show a difference in the AD risk. After adjusting for age, the interaction between ApoE4 and amyloid-associated depression (β=+0.113, SE=0.047, P=0.02) and the interaction between ApoE4 and antidepressant use (β=+0.174, SE=0.064, P=0.007) were associated with the AD risk. Conclusions Amyloid-associated depression may be prodromal depression of AD especially in the presence of ApoE4. Future studies with a larger cohort and a longer follow-up are warranted to further confirm this conclusion.

Objective: To develop a prognostic model for predicting mortality at time of extracorporeal membrane oxygenation (ECMO) initiation for children which is important for determining centerspecific risk-adjusted outcomes.Design: Multivariable logistic regression using a large national cohort of pediatric ECMO patients. Setting:The intensive care units of the eight tertiary care children's hospitals of the Collaborative Pediatric Critical Care Research Network Patients: 514 children (< 19 years), enrolled with an initial ECMO run for any indication between January 2012 and September 2014. Interventions: NoneMeasurements and Main Results: A total of 514 first ECMO runs were analyzed with an overall mortality of 45% (n=232). Weighted logistic regression was used for model selection and internal validation was performed using cross validation. The variables included in the Pediatric ECMO Prediction (PEP) model were age (pre-term neonate, full-term neonate, infant, child, and adolescent), indication for ECMO (extracorporeal cardiopulmonary resuscition, cardiac, or respiratory), meconium aspiration, congenital diaphragmatic hernia, documented blood stream infection, arterial blood pH, partial thromboplastin time, and international normalized ratio. The highest risk of mortality was associated with the presence of a documented blood stream infection (OR 5.26; CI 1.90-14.57) followed by extracorporeal cardiopulmonary resuscitation (OR = 4.36;). The c-statistic was 0.75 (95% CI, 0.70-0.80). Conclusions:The PEP model represents a model for predicting in-hospital mortality among children receiving ECMO support for any indication. Consequently, it holds promise as the first comprehensive pediatric ECMO risk stratification model which is important for benchmarking ECMO outcomes across many centers.

Amylin, a pancreatic peptide that readily crosses the blood brain barrier (BBB), and amyloid-beta peptide (Aβ), the main component of amyloid plaques and a major component of Alzheimer's disease (AD) pathology in the brain, share several features. These include having similar β-sheet secondary structures, binding to the same receptor, and being degraded by the same protease. Thus, amylin may be associated with Aβ, but the nature of their relationship remains unclear. In this study, we used human samples to study the relationship between plasma amylin and Aβ in the context of the apolipoprotein E alleles (ApoE). We found that concentrations of Aβ1-42 (P<0.0001) and Aβ1-40 (P<0.0001) increased with each quartile increase of amylin. Using multivariate regression analysis, the study sample showed that plasma amylin was associated with Aβ1-42 (β = +0.149, SE = 0.025, P<0.0001) and Aβ1-40 (β = +0.034, SE = 0.016, P = 0.04) as an outcome after adjusting for age, gender, ethnicity, ApoE4, BMI, diabetes, stroke, kidney function and lipid profile. This positive association between amylin and Aβ1-42 in plasma was found regardless of the ApoE genotype. In contrast, the relationship between amylin and Aβ1-40 in plasma seen in ApoE4 non-carriers disappeared in the presence of ApoE4. Using AD mouse models, our recent study demonstrates that intraperitoneal (i.p.) injection of synthetic amylin enhances the removal of Aβ from the brain into blood, thus resulting in increased blood levels of both amylin and Aβ. The positive association between amylin and Aβ, especially Aβ1-42, in human blood samples is probably relevant to the findings in the AD mouse models. The presence of ApoE4 may attenuate amylin's capacity to remove Aβ, especially Aβ1-40, from the AD brain.