@article{ref1,
title="Identifying those at risk for COVID-19 related suicide. Response to "Hyper/neuroinflammation in COVID-19 and suicide etiopathogenesis: hypothesis for a nefarious collision?"",
journal="Neuroscience and biobehavioral reviews",
year="2022",
author="Goldstein, Mark R. and Mascitelli, Luca",
volume="ePub",
number="ePub",
pages="ePub-ePub",
abstract="Regarding the interesting paper in this Journal (https://doi.org/10.1016/j.neubiorev.2022.104606), Costanza and coauthors mentioned the increase in suicidal ideation and suicidal behavior reported during the initial phase of the Coronavirus Disease 2019 (COVID-19) pandemic and that it possibly was related to various psychosocial factors and pre-existing psychiatric illness, while the increase in suicide risk seen during later phases of the pandemic was fueled by a pathological hyperinflammatory state, initiated by the virus causing COVID-19, the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). As such, SARS-CoV-2 activated macrophages and mast cells in the periphery and macrophages and glial cells in the brain release a myriad of inflammatory factors including IL1, IL6, and TNFα. Moreover, the authors pointed out that a similar inflammatory signature has been associated with suicide risk and posited that neuroinflammation from COVID-19 is overlapped with that of suicide pathophysiology. However, can we better identify those at higher risk for COVID-19 associated suicide?....<p /> <p>Language: en</p>",
language="en",
issn="0149-7634",
doi="10.1016/j.neubiorev.2022.104785",
url="http://dx.doi.org/10.1016/j.neubiorev.2022.104785"
}