Accuracy of US CDC COVID-19 forecasting models.

Accurate predictive modeling of pandemics is essential for optimally distributing biomedical resources and setting policy. Dozens of case prediction models have been proposed but their accuracy over time and by model type remains unclear. In this study, we systematically analyze all US CDC COVID-19 forecasting models, by first categorizing them and then calculating their mean absolute percent error, both wave-wise and on the complete timeline.

COVID-19 activity risk calculator as a gamified public health intervention tool.

The Coronavirus disease 2019 (COVID-19) pandemic, caused by the virus severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has impacted over 200 countries leading to hospitalizations and deaths of millions of people. Public health interventions, such as risk estimators, can reduce the spread of pandemics and epidemics through influencing behavior, which impacts risk of exposure and infection. Current publicly available COVID-19 risk estimation tools have had variable effectiveness during the pandemic due to their dependency on rapidly evolving factors such as community transmission levels and variants.

Using survey data to estimate the impact of the omicron variant on vaccine efficacy against COVID-19 infection.

Symptoms-based detection of SARS-CoV-2 infection is not a substitute for precise diagnostic tests but can provide insight into the likely level of infection in a given population. This study uses symptoms data collected in the Global COVID-19 Trends and Impact Surveys (UMD Global CTIS), and data on variants sequencing from GISAID. This work, conducted in January of 2022 during the emergence of the Omicron variant (subvariant BA.

Rate of brain aging and are synergistic risk factors for Alzheimer's disease.

Advanced age and the allele are the two biggest risk factors for Alzheimer's disease (AD) and declining cognitive function. We describe a universal gauge to measure molecular brain age using transcriptome analysis of four human postmortem cohorts (n = 673, ages 25-97) free of neurological disease. In a fifth cohort of older subjects with or without neurological disease (n = 438, ages 67-108), we show that subjects with brains deviating in the older direction from what would be expected based on chronological age show an increase in AD, Parkinson's disease, and cognitive decline.

Nicotine promotes neuron survival and partially protects from Parkinson's disease by suppressing SIRT6.

Parkinson's disease is characterized by progressive death of dopaminergic neurons, leading to motor and cognitive dysfunction. Epidemiological studies consistently show that the use of tobacco reduces the risk of Parkinson's. We report that nicotine reduces the abundance of SIRT6 in neuronal culture and brain tissue.

Avoiding a lost generation of scientists.

By sharing their experiences, early-career scientists can help to make the case for increased government funding for researchers.

Between destiny and disease: genetics and molecular pathways of human central nervous system aging.

Aging of the human brain is associated with "normal" functional, structural, and molecular changes that underlie alterations in cognition, memory, mood and motor function, amongst other processes. Normal aging also imposes a robust constraint on the onset of many neurological diseases, ranging from late onset neurodegenerative diseases, such as Alzheimer's (AD) and Parkinson's diseases (PD), to early onset psychiatric disorders, such as bipolar disorder (BPD) and schizophrenia (SCZ). The molecular mechanisms and genetic underpinnings of age-related changes in the brain are understudied, and, while they share some overlap with peripheral mechanisms of aging, many are unique to the largely non-mitotic brain.

Brain molecular aging, promotion of neurological disease and modulation by sirtuin 5 longevity gene polymorphism.

Mechanisms determining characteristic age-of-onset for neurological diseases are largely unknown. Normal brain aging associates with robust and progressive transcriptome changes ("molecular aging"), but the intersection with disease pathways is mostly uncharacterized. Here, using cross-cohort microarray analysis of four human brain areas, we show that neurological disease pathways largely overlap with molecular aging and that subjects carrying a newly-characterized low-expressing polymorphism in a putative longevity gene (Sirtuin5; SIRT5(prom2)) have older brain molecular ages.