Funded Projects

The onset of the COVID-19 pandemic has led to a subset of patients that, once recovered from the acute infection, also experience an intractable and debilitating set of lingering symptoms. Recent evidence shows that a range of persistent or new symptoms can manifest after 4-12 weeks in a subset of patients who have recovered from acute SARS-CoV-2 infection, and this condition has been coined long COVID by COVID-19 survivors among social support groups. Like the acute form, long COVID has multisystemic aspects. Patients can manifest with a very heterogeneous multitude of symptoms, including fatigue, post-exertional malaise, dyspnea, cognitive impairment, sleep disturbances, anxiety and depression, muscle pain, brain fog, anosmia/dysgeusia, headache, and limitation of functional capacity, which impact their quality of life. Because of the extreme clinical heterogeneity, and also due to the lack of a shared, specific definition, it is very difficult to know the real prevalence and incidence of this condition. Risk factors for developing long COVID include female sex, initial severity, and comorbidities. The mechanisms behind this syndrome have proven elusive because patients varied in symptom severity and treatment regimen including different requirements for hospitalization, supplemental oxygen, dexamethasone and remdesivir. Thus, it is critical to characterize the neurological alterations in the long COVID to prevent potential long-term health consequences. Globally, with the re-emergence of new waves, the population of people infected with long COVID continues to expand rapidly. In the current pilot proposal, we will characterize the structural microglia activation in long COVID syndrome patients and compare to non-long COVID survivors and healthy controls. Our current understanding of neurological involvement in COVID-19 supports at least three basic mechanisms for neurological findings in long-COVID, none of which are mutually exclusive. First, there is evidenc