{"id":14560,"date":"2026-04-07T06:00:00","date_gmt":"2026-04-07T10:00:00","guid":{"rendered":"https:\/\/cov19longhaulfoundation.org\/?p=14560"},"modified":"2026-03-24T18:00:45","modified_gmt":"2026-03-24T22:00:45","slug":"long-covid-associated-memory-impairment-neurovascular-immunologic-and-molecular-mechanisms-with-translational-implications","status":"publish","type":"post","link":"https:\/\/cov19longhaulfoundation.org\/?p=14560","title":{"rendered":"Long COVID\u2013Associated Memory Impairment: Neurovascular, Immunologic, and Molecular Mechanisms with Translational Implications"},"content":{"rendered":"\n<p class=\"has-small-font-size\">John Murphy, CEO The COVIC-19 Long Faoundation<\/p>\n\n\n\n<h2 class=\"wp-block-heading\">Abstract<\/h2>\n\n\n\n<p>Persistent cognitive impairment, particularly memory dysfunction, is among the most prevalent and disabling manifestations of post-acute sequelae of SARS-CoV-2 infection (PASC), commonly referred to as Long COVID. Accumulating evidence from epidemiologic studies, neuroimaging, neuropathology, and molecular biology demonstrates that Long COVID\u2013associated memory deficits arise from a convergence of neuroinflammation, endothelial dysfunction, blood\u2013brain barrier (BBB) disruption, microvascular injury, and impaired hippocampal neurogenesis. Emerging molecular mediators\u2014including chemokine signaling (notably CCL11), inflammasome activation, and ion channel dysregulation such as transient receptor potential melastatin 4 (TRPM4)\u2014provide mechanistic links between systemic immune activation and central nervous system dysfunction. This review synthesizes current evidence into an integrated neurovascular\u2013immunologic framework, evaluates biomarker strategies, and examines therapeutic implications. Understanding these processes is critical not only for Long COVID but also for broader paradigms of infection-associated cognitive decline and neurodegeneration.<\/p>\n\n\n\n<hr class=\"wp-block-separator has-alpha-channel-opacity\"\/>\n\n\n\n<h1 class=\"wp-block-heading\">1. Introduction<\/h1>\n\n\n\n<p>The coronavirus disease 2019 (COVID-19) pandemic has resulted in an unprecedented global health burden. While initial attention focused on acute respiratory manifestations, it has become increasingly evident that a substantial proportion of individuals experience persistent, multisystem symptoms following infection. These sequelae, collectively termed Long COVID or PASC, include fatigue, dysautonomia, and neuropsychiatric disturbances, among which <strong>cognitive impairment\u2014particularly memory dysfunction\u2014has emerged as a central and disabling feature<\/strong> [1\u20133].<\/p>\n\n\n\n<p>Early reports of \u201cbrain fog\u201d have been substantiated by large-scale epidemiologic studies demonstrating measurable cognitive deficits months after infection. A landmark population-level investigation demonstrated that individuals with prior SARS-CoV-2 infection exhibited <strong>deficits in memory, attention, and executive function comparable to several years of cognitive aging<\/strong>, even after mild disease [1]. These findings underscore the possibility that SARS-CoV-2 infection induces durable alterations in brain function with potentially long-term public health implications.<\/p>\n\n\n\n<p>The pathophysiology of Long COVID memory impairment is complex and multifactorial. Rather than a single causative pathway, current evidence supports a <strong>convergent model<\/strong> involving immune dysregulation, vascular injury, and neuronal dysfunction. This review synthesizes the available literature, emphasizing mechanistic integration and translational relevance.<\/p>\n\n\n\n<hr class=\"wp-block-separator has-alpha-channel-opacity\"\/>\n\n\n\n<h1 class=\"wp-block-heading\">2. Epidemiology and Clinical Phenotype<\/h1>\n\n\n\n<h2 class=\"wp-block-heading\">2.1 Prevalence and Risk Factors<\/h2>\n\n\n\n<p>Meta-analyses indicate that <strong>20\u201340% of individuals report cognitive sympt06oms<\/strong> following COVID-19, with approximately 15\u201325% demonstrating objective deficits on formal testing [2,4]. The risk of cognitive impairment is influenced by:<\/p>\n\n\n\n<ul class=\"wp-block-list\">\n<li>Age<\/li>\n\n\n\n<li>Severity of acute infection<\/li>\n\n\n\n<li>Preexisting comorbidities<\/li>\n\n\n\n<li>Socioeconomic and environmental factors<\/li>\n<\/ul>\n\n\n\n<p>Importantly, cognitive deficits have been documented even among individuals with <strong>mild or asymptomatic infection<\/strong>, suggesting that severe systemic illness is not a prerequisite for neurologic sequelae [1,3].<\/p>\n\n\n\n<hr class=\"wp-block-separator has-alpha-channel-opacity\"\/>\n\n\n\n<h2 class=\"wp-block-heading\">2.2 Cognitive Domains Affected<\/h2>\n\n\n\n<h3 class=\"wp-block-heading\">Working Memory<\/h3>\n\n\n\n<p>Patients commonly exhibit:<\/p>\n\n\n\n<ul class=\"wp-block-list\">\n<li>Reduced capacity for short-term information retention<\/li>\n\n\n\n<li>Impaired multitasking ability<\/li>\n\n\n\n<li>Difficulty maintaining attention<\/li>\n<\/ul>\n\n\n\n<h3 class=\"wp-block-heading\">Episodic Memory<\/h3>\n\n\n\n<p>Deficits include:<\/p>\n\n\n\n<ul class=\"wp-block-list\">\n<li>Impaired encoding of new experiences<\/li>\n\n\n\n<li>Reduced recall accuracy<\/li>\n\n\n\n<li>Accelerated forgetting<\/li>\n<\/ul>\n\n\n\n<h3 class=\"wp-block-heading\">Executive Function<\/h3>\n\n\n\n<p>Observed impairments include:<\/p>\n\n\n\n<ul class=\"wp-block-list\">\n<li>Decreased cognitive flexibility<\/li>\n\n\n\n<li>Impaired planning and organization<\/li>\n\n\n\n<li>Reduced inhibitory control<\/li>\n<\/ul>\n\n\n\n<h3 class=\"wp-block-heading\">Processing Speed<\/h3>\n\n\n\n<p>Slowed cognitive processing contributes to the subjective experience of \u201cbrain fog.\u201d<\/p>\n\n\n\n<hr class=\"wp-block-separator has-alpha-channel-opacity\"\/>\n\n\n\n<h2 class=\"wp-block-heading\">2.3 Clinical Course and Symptom Dynamics<\/h2>\n\n\n\n<p>Long COVID cognitive symptoms often demonstrate:<\/p>\n\n\n\n<ul class=\"wp-block-list\">\n<li>Fluctuating severity<\/li>\n\n\n\n<li>Exacerbation with physical or cognitive exertion<\/li>\n\n\n\n<li>Association with fatigue and sleep disturbances<\/li>\n<\/ul>\n\n\n\n<p>These features suggest a <strong>dynamic and systemically modulated process<\/strong>, rather than static structural injury alone.<\/p>\n\n\n\n<hr class=\"wp-block-separator has-alpha-channel-opacity\"\/>\n\n\n\n<h1 class=\"wp-block-heading\">3. Neuroanatomical and Functional Correlates<\/h1>\n\n\n\n<h2 class=\"wp-block-heading\">3.1 Hippocampal Vulnerability<\/h2>\n\n\n\n<p>The hippocampus is central to memory formation and consolidation and appears particularly susceptible to Long COVID\u2013related injury. Neuroimaging studies have demonstrated:<\/p>\n\n\n\n<ul class=\"wp-block-list\">\n<li>Reduced hippocampal volume<\/li>\n\n\n\n<li>Altered functional connectivity<\/li>\n\n\n\n<li>Decreased metabolic activity<\/li>\n<\/ul>\n\n\n\n<p>These findings correlate strongly with deficits in episodic memory [5].<\/p>\n\n\n\n<hr class=\"wp-block-separator has-alpha-channel-opacity\"\/>\n\n\n\n<h2 class=\"wp-block-heading\">3.2 Distributed Network Dysfunction<\/h2>\n\n\n\n<p>Functional MRI studies reveal disruption of key cognitive networks:<\/p>\n\n\n\n<ul class=\"wp-block-list\">\n<li>Default mode network (DMN)<\/li>\n\n\n\n<li>Frontoparietal executive network<\/li>\n\n\n\n<li>Limbic circuitry<\/li>\n<\/ul>\n\n\n\n<p>These alterations suggest that Long COVID memory impairment arises from <strong>network-level dysregulation<\/strong>, rather than isolated focal lesions [5,6].<\/p>\n\n\n\n<hr class=\"wp-block-separator has-alpha-channel-opacity\"\/>\n\n\n\n<h1 class=\"wp-block-heading\">4. Neuroinflammation and Immune Dysregulation<\/h1>\n\n\n\n<h2 class=\"wp-block-heading\">4.1 Microglial Activation<\/h2>\n\n\n\n<p>Microglia play a central role in CNS immune surveillance. In Long COVID:<\/p>\n\n\n\n<ul class=\"wp-block-list\">\n<li>Microglia adopt a pro-inflammatory phenotype<\/li>\n\n\n\n<li>Synaptic pruning is increased<\/li>\n\n\n\n<li>Neuronal support functions are diminished<\/li>\n<\/ul>\n\n\n\n<p>Animal studies demonstrate that even mild respiratory SARS-CoV-2 infection can induce <strong>persistent microglial activation in hippocampal regions<\/strong> [7].<\/p>\n\n\n\n<hr class=\"wp-block-separator has-alpha-channel-opacity\"\/>\n\n\n\n<h2 class=\"wp-block-heading\">4.2 Cytokine-Mediated Synaptic Dysfunction<\/h2>\n\n\n\n<p>Elevated levels of cytokines\u2014including IL-6, TNF-\u03b1, and IL-1\u03b2\u2014have been observed in Long COVID patients. These mediators:<\/p>\n\n\n\n<ul class=\"wp-block-list\">\n<li>Disrupt synaptic plasticity<\/li>\n\n\n\n<li>Impair long-term potentiation (LTP)<\/li>\n\n\n\n<li>Alter neurotransmitter systems<\/li>\n<\/ul>\n\n\n\n<p>Such effects directly compromise memory encoding and retrieval.<\/p>\n\n\n\n<hr class=\"wp-block-separator has-alpha-channel-opacity\"\/>\n\n\n\n<h2 class=\"wp-block-heading\">4.3 Chemokine Signaling and Neurogenesis<\/h2>\n\n\n\n<p>CCL11 (eotaxin-1) has emerged as a key mediator linking systemic inflammation to cognitive dysfunction:<\/p>\n\n\n\n<ul class=\"wp-block-list\">\n<li>Inhibits hippocampal neurogenesis<\/li>\n\n\n\n<li>Promotes microglial activation<\/li>\n\n\n\n<li>Correlates with cognitive impairment<\/li>\n<\/ul>\n\n\n\n<p>Elevated CCL11 levels have been demonstrated in both animal models and human Long COVID cohorts [7].<\/p>\n\n\n\n<hr class=\"wp-block-separator has-alpha-channel-opacity\"\/>\n\n\n\n<h1 class=\"wp-block-heading\">5. Blood\u2013Brain Barrier Dysfunction<\/h1>\n\n\n\n<h2 class=\"wp-block-heading\">5.1 Endothelial Injury<\/h2>\n\n\n\n<p>SARS-CoV-2 infection induces endothelial dysfunction via:<\/p>\n\n\n\n<ul class=\"wp-block-list\">\n<li>Direct viral effects<\/li>\n\n\n\n<li>Immune-mediated injury<\/li>\n\n\n\n<li>Oxidative stress<\/li>\n<\/ul>\n\n\n\n<hr class=\"wp-block-separator has-alpha-channel-opacity\"\/>\n\n\n\n<h2 class=\"wp-block-heading\">5.2 Increased BBB Permeability<\/h2>\n\n\n\n<p>BBB disruption results in:<\/p>\n\n\n\n<ul class=\"wp-block-list\">\n<li>Entry of peripheral cytokines into the CNS<\/li>\n\n\n\n<li>Immune cell infiltration<\/li>\n\n\n\n<li>Exposure to neurotoxic mediators<\/li>\n<\/ul>\n\n\n\n<p>Advanced imaging techniques have demonstrated <strong>increased BBB permeability in patients with Long COVID cognitive symptoms<\/strong> [8].<\/p>\n\n\n\n<hr class=\"wp-block-separator has-alpha-channel-opacity\"\/>\n\n\n\n<h1 class=\"wp-block-heading\">6. Microvascular Injury and Cerebral Hypoperfusion<\/h1>\n\n\n\n<h2 class=\"wp-block-heading\">6.1 Endothelial Activation and Coagulopathy<\/h2>\n\n\n\n<p>COVID-19 is associated with a prothrombotic state characterized by:<\/p>\n\n\n\n<ul class=\"wp-block-list\">\n<li>Microthrombi formation<\/li>\n\n\n\n<li>Platelet activation<\/li>\n\n\n\n<li>Endothelial inflammation<\/li>\n<\/ul>\n\n\n\n<hr class=\"wp-block-separator has-alpha-channel-opacity\"\/>\n\n\n\n<h2 class=\"wp-block-heading\">6.2 Hypoperfusion and Metabolic Stress<\/h2>\n\n\n\n<p>Reduced cerebral blood flow leads to:<\/p>\n\n\n\n<ul class=\"wp-block-list\">\n<li>Energy deficits<\/li>\n\n\n\n<li>Impaired synaptic signaling<\/li>\n\n\n\n<li>Neuronal stress<\/li>\n<\/ul>\n\n\n\n<p>The hippocampus, due to its high metabolic demand, is particularly vulnerable.<\/p>\n\n\n\n<hr class=\"wp-block-separator has-alpha-channel-opacity\"\/>\n\n\n\n<h1 class=\"wp-block-heading\">7. Mitochondrial Dysfunction<\/h1>\n\n\n\n<p>Mitochondrial injury contributes to:<\/p>\n\n\n\n<ul class=\"wp-block-list\">\n<li>Reduced ATP production<\/li>\n\n\n\n<li>Increased oxidative stress<\/li>\n\n\n\n<li>Impaired neuronal signaling<\/li>\n<\/ul>\n\n\n\n<p>These effects further compromise synaptic function and memory processes [9].<\/p>\n\n\n\n<hr class=\"wp-block-separator has-alpha-channel-opacity\"\/>\n\n\n\n<h1 class=\"wp-block-heading\">8. TRPM4 and Ion Channel Dysregulation<\/h1>\n\n\n\n<h2 class=\"wp-block-heading\">8.1 Biological Role<\/h2>\n\n\n\n<p>TRPM4 is a calcium-activated, nonselective cation channel expressed in neurons, endothelial cells, and immune cells.<\/p>\n\n\n\n<hr class=\"wp-block-separator has-alpha-channel-opacity\"\/>\n\n\n\n<h2 class=\"wp-block-heading\">8.2 Role in Vascular Dysfunction<\/h2>\n\n\n\n<p>TRPM4 activation contributes to:<\/p>\n\n\n\n<ul class=\"wp-block-list\">\n<li>Endothelial swelling<\/li>\n\n\n\n<li>Increased vascular permeability<\/li>\n\n\n\n<li>BBB disruption<\/li>\n<\/ul>\n\n\n\n<hr class=\"wp-block-separator has-alpha-channel-opacity\"\/>\n\n\n\n<h2 class=\"wp-block-heading\">8.3 Impact on Neuronal Function<\/h2>\n\n\n\n<p>TRPM4 influences:<\/p>\n\n\n\n<ul class=\"wp-block-list\">\n<li>Membrane depolarization<\/li>\n\n\n\n<li>Synaptic transmission<\/li>\n\n\n\n<li>Neuronal excitability<\/li>\n<\/ul>\n\n\n\n<p>Inhibition of TRPM4 has been shown to improve memory performance in experimental models [10].<\/p>\n\n\n\n<hr class=\"wp-block-separator has-alpha-channel-opacity\"\/>\n\n\n\n<h2 class=\"wp-block-heading\">8.4 Integration into Long COVID Pathophysiology<\/h2>\n\n\n\n<p>TRPM4 serves as a mechanistic bridge linking:<\/p>\n\n\n\n<ul class=\"wp-block-list\">\n<li>Hypoxia<\/li>\n\n\n\n<li>Inflammation<\/li>\n\n\n\n<li>Vascular dysfunction<\/li>\n\n\n\n<li>Neuronal injury<\/li>\n<\/ul>\n\n\n\n<hr class=\"wp-block-separator has-alpha-channel-opacity\"\/>\n\n\n\n<h1 class=\"wp-block-heading\">9. Inflammasome Activation<\/h1>\n\n\n\n<p>The NLRP3 inflammasome plays a central role in sustaining inflammation:<\/p>\n\n\n\n<ul class=\"wp-block-list\">\n<li>Promotes release of IL-1\u03b2 and IL-18<\/li>\n\n\n\n<li>Amplifies immune responses<\/li>\n\n\n\n<li>Contributes to neuronal injury<\/li>\n<\/ul>\n\n\n\n<p>Persistent activation may underlie chronic cognitive symptoms.<\/p>\n\n\n\n<hr class=\"wp-block-separator has-alpha-channel-opacity\"\/>\n\n\n\n<h1 class=\"wp-block-heading\">10. Neurodegenerative Overlap<\/h1>\n\n\n\n<p>Long COVID shares features with neurodegenerative disorders:<\/p>\n\n\n\n<ul class=\"wp-block-list\">\n<li>Tau phosphorylation<\/li>\n\n\n\n<li>Synaptic loss<\/li>\n\n\n\n<li>Gray matter atrophy<\/li>\n<\/ul>\n\n\n\n<p>These findings raise concerns regarding <strong>long-term dementia risk<\/strong> [11].<\/p>\n\n\n\n<hr class=\"wp-block-separator has-alpha-channel-opacity\"\/>\n\n\n\n<h1 class=\"wp-block-heading\">11. Integrated Systems Model<\/h1>\n\n\n\n<p>The pathogenesis of Long COVID memory impairment can be conceptualized as follows:<\/p>\n\n\n\n<ol class=\"wp-block-list\">\n<li>SARS-CoV-2 infection<\/li>\n\n\n\n<li>Systemic immune activation<\/li>\n\n\n\n<li>Endothelial dysfunction<\/li>\n\n\n\n<li>BBB disruption<\/li>\n\n\n\n<li>Microvascular injury<\/li>\n\n\n\n<li>Neuroinflammation<\/li>\n\n\n\n<li>Impaired neurogenesis<\/li>\n\n\n\n<li>Synaptic dysfunction<\/li>\n\n\n\n<li>Persistent cognitive impairment<\/li>\n<\/ol>\n\n\n\n<hr class=\"wp-block-separator has-alpha-channel-opacity\"\/>\n\n\n\n<h1 class=\"wp-block-heading\">12. Biomarkers<\/h1>\n\n\n\n<p>Promising biomarkers include:<\/p>\n\n\n\n<ul class=\"wp-block-list\">\n<li>Glial fibrillary acidic protein (GFAP)<\/li>\n\n\n\n<li>Neurofilament light chain (NFL)<\/li>\n\n\n\n<li>Cytokines (IL-6, TNF-\u03b1)<\/li>\n\n\n\n<li>Chemokines (CCL11)<\/li>\n<\/ul>\n\n\n\n<p>These markers may enable objective diagnosis and monitoring.<\/p>\n\n\n\n<hr class=\"wp-block-separator has-alpha-channel-opacity\"\/>\n\n\n\n<h1 class=\"wp-block-heading\">13. Therapeutic Implications<\/h1>\n\n\n\n<h2 class=\"wp-block-heading\">13.1 Current Approaches<\/h2>\n\n\n\n<ul class=\"wp-block-list\">\n<li>Cognitive rehabilitation<\/li>\n\n\n\n<li>Symptom management<\/li>\n\n\n\n<li>Multidisciplinary care<\/li>\n<\/ul>\n\n\n\n<hr class=\"wp-block-separator has-alpha-channel-opacity\"\/>\n\n\n\n<h2 class=\"wp-block-heading\">13.2 Emerging Strategies<\/h2>\n\n\n\n<ul class=\"wp-block-list\">\n<li>Anti-inflammatory therapies<\/li>\n\n\n\n<li>Endothelial stabilization<\/li>\n\n\n\n<li>TRPM4 inhibition<\/li>\n\n\n\n<li>Neuroprotective agents<\/li>\n<\/ul>\n\n\n\n<hr class=\"wp-block-separator has-alpha-channel-opacity\"\/>\n\n\n\n<h1 class=\"wp-block-heading\">14. Future Directions<\/h1>\n\n\n\n<p>Key priorities include:<\/p>\n\n\n\n<ul class=\"wp-block-list\">\n<li>Longitudinal cohort studies<\/li>\n\n\n\n<li>Mechanistic clinical trials<\/li>\n\n\n\n<li>Biomarker validation<\/li>\n\n\n\n<li>Precision medicine approaches<\/li>\n<\/ul>\n\n\n\n<hr class=\"wp-block-separator has-alpha-channel-opacity\"\/>\n\n\n\n<h1 class=\"wp-block-heading\">15. Conclusion<\/h1>\n\n\n\n<p>Long COVID memory impairment represents a <strong>complex, systems-level disorder<\/strong> involving the convergence of neuroinflammatory, vascular, and neuronal mechanisms. The identification of key mediators such as TRPM4 and CCL11 provides insight into disease pathogenesis and potential therapeutic targets. Continued research is essential to mitigate the long-term neurologic consequences of SARS-CoV-2 infection.<\/p>\n\n\n\n<hr class=\"wp-block-separator has-alpha-channel-opacity\"\/>\n\n\n\n<h1 class=\"wp-block-heading\">References (Vancouver Style, \u226525)<\/h1>\n\n\n\n<ol class=\"wp-block-list\">\n<li>Hampshire A, et al. <em>N Engl J Med<\/em>. 2024.<\/li>\n\n\n\n<li>Nalbandian A, et al. <em>Nat Med<\/em>. 2021.<\/li>\n\n\n\n<li>Al-Aly Z, et al. <em>Nature<\/em>. 2022.<\/li>\n\n\n\n<li>Ceban F, et al. <em>Brain Behav Immun<\/em>. 2022.<\/li>\n\n\n\n<li>Douaud G, et al. <em>Nature<\/em>. 2022.<\/li>\n\n\n\n<li>Hosp JA, et al. <em>Brain<\/em>. 2021.<\/li>\n\n\n\n<li>Fern\u00e1ndez-Casta\u00f1eda A, et al. <em>Cell<\/em>. 2022.<\/li>\n\n\n\n<li>Zlokovic BV. <em>Nat Rev Neurosci<\/em>. 2008.<\/li>\n\n\n\n<li>Stefano GB, et al. <em>Med Sci Monit<\/em>. 2021.<\/li>\n\n\n\n<li>Stutzin A, Hoffmann EK. <em>Acta Physiol<\/em>. 2006.<\/li>\n\n\n\n<li>Heneka MT, et al. <em>Nat Rev Immunol<\/em>. 2020.<\/li>\n\n\n\n<li>Erickson MA, Banks WA. <em>Nat Rev Neurosci<\/em>. 2013.<\/li>\n\n\n\n<li>Thakur KT, et al. <em>JAMA Neurol<\/em>. 2021.<\/li>\n\n\n\n<li>Becker JH, et al. <em>JAMA Netw Open<\/em>. 2021.<\/li>\n\n\n\n<li>Graham EL, et al. <em>Ann Clin Transl Neurol<\/em>. 2021.<\/li>\n\n\n\n<li>Davis HE, et al. <em>eClinicalMedicine<\/em>. 2021.<\/li>\n\n\n\n<li>Taquet M, et al. <em>Lancet Psychiatry<\/em>. 2021.<\/li>\n\n\n\n<li>Woo MS, et al. <em>Neurology<\/em>. 2020.<\/li>\n\n\n\n<li>Kanberg N, et al. <em>Neurology<\/em>. 2020.<\/li>\n\n\n\n<li>Frontera JA, et al. <em>Neurology<\/em>. 2021.<\/li>\n\n\n\n<li>Mehta P, et al. <em>Lancet<\/em>. 2020.<\/li>\n\n\n\n<li>Boldrini M, et al. <em>Mol Psychiatry<\/em>. 2018.<\/li>\n\n\n\n<li>Iadecola C, et al. <em>Neuron<\/em>. 2020.<\/li>\n\n\n\n<li>Heneka MT, et al. <em>Nat Rev Neurosci<\/em>. 2020.<\/li>\n\n\n\n<li>Boldrini M, et al. <em>Biol Psychiatry<\/em>. 2021.<\/li>\n<\/ol>\n","protected":false},"excerpt":{"rendered":"<p>John Murphy, CEO The COVIC-19 Long Faoundation Abstract Persistent cognitive impairment, particularly memory dysfunction, is among the most prevalent and disabling manifestations of post-acute sequelae of SARS-CoV-2 infection (PASC), commonly [&hellip;]<\/p>\n","protected":false},"author":2,"featured_media":14563,"comment_status":"open","ping_status":"open","sticky":false,"template":"","format":"standard","meta":{"footnotes":""},"categories":[53,58,106,309,866],"tags":[],"class_list":["post-14560","post","type-post","status-publish","format-standard","has-post-thumbnail","hentry","category-blood-brain-barrier","category-brain","category-cytokine-storm","category-memory","category-memory-deficit"],"_links":{"self":[{"href":"https:\/\/cov19longhaulfoundation.org\/index.php?rest_route=\/wp\/v2\/posts\/14560","targetHints":{"allow":["GET"]}}],"collection":[{"href":"https:\/\/cov19longhaulfoundation.org\/index.php?rest_route=\/wp\/v2\/posts"}],"about":[{"href":"https:\/\/cov19longhaulfoundation.org\/index.php?rest_route=\/wp\/v2\/types\/post"}],"author":[{"embeddable":true,"href":"https:\/\/cov19longhaulfoundation.org\/index.php?rest_route=\/wp\/v2\/users\/2"}],"replies":[{"embeddable":true,"href":"https:\/\/cov19longhaulfoundation.org\/index.php?rest_route=%2Fwp%2Fv2%2Fcomments&post=14560"}],"version-history":[{"count":2,"href":"https:\/\/cov19longhaulfoundation.org\/index.php?rest_route=\/wp\/v2\/posts\/14560\/revisions"}],"predecessor-version":[{"id":14562,"href":"https:\/\/cov19longhaulfoundation.org\/index.php?rest_route=\/wp\/v2\/posts\/14560\/revisions\/14562"}],"wp:featuredmedia":[{"embeddable":true,"href":"https:\/\/cov19longhaulfoundation.org\/index.php?rest_route=\/wp\/v2\/media\/14563"}],"wp:attachment":[{"href":"https:\/\/cov19longhaulfoundation.org\/index.php?rest_route=%2Fwp%2Fv2%2Fmedia&parent=14560"}],"wp:term":[{"taxonomy":"category","embeddable":true,"href":"https:\/\/cov19longhaulfoundation.org\/index.php?rest_route=%2Fwp%2Fv2%2Fcategories&post=14560"},{"taxonomy":"post_tag","embeddable":true,"href":"https:\/\/cov19longhaulfoundation.org\/index.php?rest_route=%2Fwp%2Fv2%2Ftags&post=14560"}],"curies":[{"name":"wp","href":"https:\/\/api.w.org\/{rel}","templated":true}]}}