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Objectives Older adults are particularly vulnerable to the negative consequences of antipsychotic exposure and are disproportionally affected by higher mortality from coronavirus disease 2019 (COVID-19). Our goal was to determine whether concurrent antipsychotic medication use was associated with increased COVID-19 mortality in older patients with preexisting behavioral health problems. We also report on findings from post-COVID follow-ups. Design Retrospective observational study. Participants Outpatients at a geriatric psychiatric clinic in New York City. Measurements Demographic and clinical data including medication, diagnosis and Clinical Global Impression Severity (CGI-S) scales on outpatients who had COVID-19 between February 28th and October 1st 2020 were extracted from the electronic health records (EHR) from the hospital. Results A total of 56 patients were diagnosed with COVID-19 (mean age 76 years; median age 75 years) and 13 (23.2%) died. We found an increased mortality risk for patients who were prescribed at least one antipsychotic medication at the time of COVID-19 infection (Fisher’s exact test P = 0.009, OR = 11.1, 95% confidence interval: 1.4–96.0). This result remains significant after adjusting for age, gender, housing context and dementia (Logistic regression P = 0.035, Beta = 2.4). Furthermore, we found that most patients who survived COVID-19 (88.4%) recovered to pre-COVID baseline in terms of psychiatric symptoms. Comparison of pre- and post-COVID assessments of CGI-S for 33 patients who recovered from COVID-19 were not significantly different. Conclusion We observed a higher COVID-19 mortality associated with concurrent antipsychotics use in older patients receiving behavioral health services. The majority of patients in our geriatric clinic who recovered from COVID-19 appeared to return to their pre-COVID psychiatric function. More precise estimates of the risk associated with antipsychotic treatment in older patients with COVID-19 and other underlying factors will come from larger datasets and meta-analyses.

To evaluate how age and apolipoprotein E-e4 (APOE4) status interact with APOE-independent polygenic risk score (PRSnon-APOE), we estimated PRSnon-APOE in superagers (age ≥ 90 years, N = 346), 89− controls (age 60–89, N = 2930), and Alzheimer's disease (AD) cases (N = 1760). Using superagers, we see a nearly 5 times greater odds ratio (OR) for AD comparing the top PRSnon-APOE decile to the lowest decile (OR = 4.82, p = 2.5 × 10−6), which is twice the OR as using 89− controls (OR = 2.38, p = 4.6 × 10−9). Thus PRSnon-APOE is correlated with age, which in turn is associated with APOE. Further exploring these relationships, we find that PRSnon-APOE modifies age at onset among APOE4 carriers, but not among noncarriers. More specifically, PRSnon-APOE in the top decile predicts an age at onset 5 years earlier compared with the lowest decile (70.1 vs. 75.0 years; t-test p = 2.4 × 10−5) among APOE4 carriers. This disproportionally large PRSnon-APOE among younger APOE4-positive cases is reflected in a significant statistical interaction between APOE4 status and age at onset (β = −0.02, p = 4.8 × 10−3) as a predictor of PRSnon-APOE. Thus, the known AD risk variants are particularly detrimental in young APOE4 carriers.

Introduction The novel coronavirus disease 2019 (COVID-19) disproportionally affects elderly patients leading to particularly high morbidity and mortality rates in this population. Age, gender, comorbidities, and housing context have been reported to be among the risk factors for mortality. Exposure to antipsychotics have been discussed to potentially impact the immune response and may pose additional risks. Furthermore, neuropsychiatric presentations are common among older patients and it is unclear how geriatric patients with preexisting psychiatric and neuropsychiatric problems recover from COVID-19. Methods In this retrospective observational study, we describe demographic characteristics of patients at a large geriatric psychiatric outpatient clinic in the New York metropolitan area, who had COVID-19. Our aim is to identify factors that may be associated with increased mortality and to evaluate whether those who survived returned to pre-COVID baseline function. We combined information provided by the treating psychiatrists with data that could be extracted from the electronic health records. Results Between February and September 2020, we identified 56 patients who were diagnosed with COVID-19 (mean age 76 years old). Thirteen patients (23.2%) died and we found that antipsychotics use at the time of COVID-19 infection is associated with increased risk of death (Fisher's exact test P= 0.009, odds ratio = 11.5, 95% confidence interval: 1.4 – 96.0). The result remains significant after adjusting for age, gender, housing context and presence of neurocognitive disorder (Logistic regression P=0.037, Beta=2.4). Furthermore, we found that most patients who survived COVID-19 recovered to baseline (88.4%) as indicated by the ratio of pre- and post-COVID Clinical Global Impressions Severity scale (mean ratio= 0.98, median=1.0, One-sample t-test P=0.48) in 33 patients. Conclusions In conclusion, antipsychotics appear to be associated with higher mortality in our geriatric psychiatry outpatient cohort. However, it is encouraging to find that the majority of elderly patients who survived COVID-19 seems to recover to their baseline neuropsychiatric function. Future larger studies are needed to put these observations into a broader context as well as to explore underlying mechanisms of risk factors. Funding NIH K08 AG054727

The purpose of this study was to examine the potential effect modifying role of the BDNF Val66Met polymorphism on the association of soccer heading with white matter microstructure. We studied 312 players enrolled in the ongoing Einstein Soccer Study, a longitudinal study of amateur soccer player in New York City and surrounding areas. At enrollment and 2 years later, total heading in the prior 12 months (12-mo.) was estimated using an established self-report instrument and diffusion tensor imaging (DTI) was performed. Generalized Estimating Equations (GEE) logistic regression models were employed to test effect modification by the BDNF Val66Met polymorphism on the association between 12-mo. heading exposure and DTI. We identified a significant interaction of 12-mo heading*BDNF Val66Met genotype on the presence of low Radial Diffusivity, a DTI marker associated with myelination. Only Met (+) players demonstrated significantly reduced odds of low RD [OR (95 % CI): −2.36 (−3.53, −1.19)] associated with the highest vs. lowest quartile of 12-mo heading exposure. BDNF Val66Met (+) soccer players with long-term exposure to high levels of heading exhibit less low Radial Diffusivity, suggesting impaired re-myelination may be a substrate of the previously reported association between heading and poor functional outcomes in soccer players.

The nonadherence rate to psychiatric medications among the geriatric patient population is estimated to be similar to that in the younger adult population, around 50%. Contributing factors to psychotropic medication nonadherence include patient-specific risk factors (for example, illness beliefs and cognitive function), drug-specific factors (for example, adverse effects and cost), as well as social factors (e.g., family support). Randomized controlled trials on geriatric adherence to psychiatric medications are scarce. We propose strategies that are better adapted to the geriatric population to improve medication adherence.

Alzheimer’s disease (AD) is the most common type of dementia, which has a substantial genetic component. AD affects predominantly older people. Accordingly, the prevalence of dementia has been rising as the population ages. To date, there are no effective interventions that can cure or halt the progression of AD. The only available treatments are the management of certain symptoms and consequences of dementia. The current state-of-the-art medical care for AD comprises three simple principles: prevent the preventable, achieve early diagnosis, and manage the manageable symptoms. This review provides a summary of the current state of knowledge of risk factors for AD, biological diagnostic testing, and prospects for treatment. Special emphasis is given to recent advances in genetics of AD and the way genomic data may support prevention, early intervention, and development of effective pharmacological treatments. Mutations in the APP, PSEN1, and PSEN2 genes cause early onset Alzheimer’s disease (EOAD) that follows a Mendelian inheritance pattern. For late onset Alzheimer’s disease (LOAD), APOE4 was identified as a major risk allele more than two decades ago. Population-based genome-wide association studies of late onset AD have now additionally identified common variants at roughly 30 genetic loci. Furthermore, rare variants (allele frequency

A functional variant in the Fc receptor-like 3 (FCRL3) gene has been implicated in susceptibility to autoimmune diseases such as rheumatoid arthritis, systemic lupus erythematosus and autoimmune thyroid disease. Investigating a large case-control sample of patients with alopecia areata (AA), we found no evidence for the involvement of FCRL3 in susceptibility to AA.