{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,30]],"date-time":"2026-08-30T02:47:40Z","timestamp":1788058060429,"version":"build-2784847793"},"reference-count":156,"publisher":"MDPI AG","issue":"16","license":[{"start":{"date-parts":[[2023,8,10]],"date-time":"2023-08-10T00:00:00Z","timestamp":1691625600000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["IJMS"],"abstract":"<jats:p>Long COVID, also called post-acute sequelae of SARS-CoV-2, is characterized by a multitude of lingering symptoms, including impaired cognition, that can last for many months. This symptom, often called \u201cbrain fog\u201d, affects the life quality of numerous individuals, increasing medical complications as well as healthcare expenditures. The etiopathogenesis of SARS-CoV-2-induced cognitive deficit is unclear, but the most likely cause is chronic inflammation maintained by a viral remnant thriving in select body reservoirs. These viral sanctuaries are likely comprised of fused, senescent cells, including microglia and astrocytes, that the pathogen can convert into neurotoxic phenotypes. Moreover, as the enteric nervous system contains neurons and glia, the virus likely lingers in the gastrointestinal tract as well, accounting for the intestinal symptoms of long COVID. Fusogens are proteins that can overcome the repulsive forces between cell membranes, allowing the virus to coalesce with host cells and enter the cytoplasm. In the intracellular compartment, the pathogen hijacks the actin cytoskeleton, fusing host cells with each other and engendering pathological syncytia. Cell\u2013cell fusion enables the virus to infect the healthy neighboring cells. We surmise that syncytia formation drives cognitive impairment by facilitating the \u201cseeding\u201d of hyperphosphorylated Tau, documented in COVID-19. In our previous work, we hypothesized that the SARS-CoV-2 virus induces premature endothelial senescence, increasing the permeability of the intestinal and blood\u2013brain barrier. This enables the migration of gastrointestinal tract microbes and\/or their components into the host circulation, eventually reaching the brain where they may induce cognitive dysfunction. For example, translocated lipopolysaccharides or microbial DNA can induce Tau hyperphosphorylation, likely accounting for memory problems. In this perspective article, we examine the pathogenetic mechanisms and potential biomarkers of long COVID, including microbial cell-free DNA, interleukin 22, and phosphorylated Tau, as well as the beneficial effect of transcutaneous vagal nerve stimulation.<\/jats:p>","DOI":"10.3390\/ijms241612648","type":"journal-article","created":{"date-parts":[[2023,8,10]],"date-time":"2023-08-10T10:11:22Z","timestamp":1691662282000},"page":"12648","update-policy":"https:\/\/doi.org\/10.3390\/mdpi_crossmark_policy","source":"Crossref","is-referenced-by-count":16,"title":["Long COVID as a Tauopathy: Of \u201cBrain Fog\u201d and \u201cFusogen Storms\u201d"],"prefix":"10.3390","volume":"24","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-2406-715X","authenticated-orcid":false,"given":"Adonis","family":"Sfera","sequence":"first","affiliation":[{"name":"Paton State Hospital, 3102 Highland Ave, Patton, CA 92369, USA"},{"name":"School of Behavioral Health, Loma Linda University, 11139 Anderson St., Loma Linda, CA 92350, USA"},{"name":"Department of Psychiatry, University of California, Riverside 900 University Ave, Riverside, CA 92521, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Leah","family":"Rahman","sequence":"additional","affiliation":[{"name":"Department of Neuroscience, University of Oregon, 222 Huestis Hall, Eugene, OR 97401, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Carlos Manuel","family":"Zapata-Mart\u00edn del Campo","sequence":"additional","affiliation":[{"name":"Instituto National de Cardiologia, Juan Badiano 1, Belisario Dom\u00ednguez Secc 16, Tlalpan, Ciudad de M\u00e9xico 14080, Mexico"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Zisis","family":"Kozlakidis","sequence":"additional","affiliation":[{"name":"International Agency for Research on Cancer, World Health Organization, 69000 Lyon, France"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1968","published-online":{"date-parts":[[2023,8,10]]},"reference":[{"key":"ref_1","doi-asserted-by":"crossref","unstructured":"Silva, M.C., and Haggarty, S.J. 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