By James Lyons-Weiler, PhD
The relationship between SARS-CoV-2 infection and mental health has often been framed too narrowly. One interpretation attributes depression, anxiety, cognitive dysfunction, sleep disruption, fatigue, and related complaints largely to the psychological burden of illness, isolation, social disruption, and pandemic stress. Another attributes these outcomes directly to the biological effects of the virus, and increasingly to the SARS-CoV-2 spike protein itself.
Neither formulation adequately represents the evidence.
Human studies have established that neurological, cognitive, and psychiatric abnormalities can follow SARS-CoV-2 infection. Experimental studies have separately demonstrated that spike protein can perturb several systems directly relevant to cognition, mood, and neurological function, including the blood-brain barrier, cerebral pericytes, microglia, astrocytes, synaptic maintenance, mitochondrial energetics, inflammatory signaling, and monoamine metabolism. The important scientific problem is therefore no longer whether spike possesses biological activity relevant to the nervous system. It does. The unresolved questions concern the magnitude, duration, anatomical distribution, and clinical importance of those effects in humans.
That distinction is critical. Human studies have not established that spike protein alone accounts for a defined proportion of post-COVID depression, anxiety, cognitive impairment, fatigue, or other neuropsychiatric outcomes. SARS-CoV-2 infection simultaneously exposes a patient to viral replication, multiple viral proteins, innate and adaptive immune responses, endothelial injury, coagulation abnormalities, autonomic disturbances, metabolic disruption, hypoxia in severe illness, and the psychological effects of acute and chronic disease. Assigning all subsequent neurological or psychiatric morbidity to a single viral component would therefore exceed the evidence.
At the same time, dismissing spike as merely an inert antigen is increasingly difficult to reconcile with the experimental literature.
The human signal is real, but it is not specific to spike
Large epidemiological studies established early in the pandemic that neurological and psychiatric diagnoses occurred at elevated frequency following SARS-CoV-2 infection. Taquet and colleagues examined 1,284,437 patients with COVID-19 and compared their subsequent neurological and psychiatric outcomes with those occurring after other respiratory infections. The trajectories differed substantially by endpoint. Excess risk for mood and anxiety disorders diminished comparatively rapidly, whereas cognitive deficit and several neurological outcomes persisted for considerably longer. That divergence is important because it demonstrates that “mental health after COVID” is not a biologically coherent endpoint. Anxiety, depression, memory impairment, executive dysfunction, sleep disturbance, fatigue, and neurological disease must be analyzed separately rather than pooled under a single convenient label.
Earlier work from the same research group, involving 236,379 COVID-19 survivors, similarly documented substantial neurological and psychiatric morbidity during the first six months after infection, with higher risks among patients who experienced more severe disease. These studies establish an association between SARS-CoV-2 infection and subsequent neuropsychiatric illness, but they cannot isolate spike protein from the numerous other exposures generated by infection.
Longer-term studies continue to find persistent abnormalities. A 2025 meta-analysis involving more than four million patients estimated pooled prevalences of 43.3% for fatigue, 27.8% for memory problems, 27.1% for cognitive impairment, 24.4% for sleep disorders, 23.8% for impaired concentration, 14.0% for depression, and 13.2% for anxiety at six months or longer. The heterogeneity was substantial across these endpoints, so these figures should not be treated as universal population risks. They instead describe averages across studies that differed in recruitment, case definition, follow-up interval, disease severity, measurement instruments, and population characteristics.
A separate 2025 meta-analysis of 94 studies involving people classified as having long COVID estimated depression at approximately 25% and anxiety at approximately 23%. Again, wide prediction intervals make clear that prevalence depends heavily on how long COVID is defined and how symptoms are measured.
The human signal is therefore difficult to dismiss. What these studies do not establish is its molecular cause.
The blood-brain barrier provides an important bridge
One of the strongest connections between the clinical literature and experimental spike research emerged from direct study of the blood-brain barrier.
Greene and colleagues reported in Nature Neuroscience that individuals with long-COVID-associated cognitive impairment showed blood-brain-barrier disruption on dynamic contrast-enhanced MRI. They also identified persistent systemic inflammation and abnormalities involving coagulation and endothelial biology. The finding matters because the blood-brain barrier is not merely a static wall separating blood from nervous tissue. It is an active neurovascular interface composed of endothelial cells, pericytes, basement membrane components, astrocytic endfeet, and interacting signaling systems that regulate the chemical environment of the brain.
Disruption of this interface can alter the entry of inflammatory mediators, plasma proteins, immune signals, and metabolites into neural tissue. The Greene study does not identify spike protein as the cause of this abnormality, but it establishes in humans the kind of neurovascular pathology that several spike experiments predict.
DeOre and colleagues tested SARS-CoV-2 spike protein in a three-dimensional blood-brain-barrier model and found that spike activated RhoA, a regulator of cytoskeletal organization and tight-junction dynamics. Inhibition of RhoA substantially rescued the spike-induced tight-junction abnormalities. This provides stronger mechanistic evidence than an association alone: a defined exposure produced a defined cellular abnormality through an identifiable pathway, and interruption of that pathway reduced the effect.
The limitation is translation. A laboratory blood-brain-barrier model cannot establish the concentration, molecular form, tissue exposure, or duration necessary to reproduce the same phenomenon in humans. What the study does establish is that spike protein possesses the intrinsic capacity to disturb neurovascular barrier biology.
Pericytes provide another plausible route to neurological dysfunction
Brain pericytes surround cerebral capillaries and participate in blood-flow regulation, blood-brain-barrier maintenance, and neurovascular signaling. Their dysfunction can therefore affect neural tissue without requiring direct neuronal infection.
Khaddaj-Mallat and colleagues exposed human brain vascular pericytes to SARS-CoV-2 spike protein and observed altered cellular morphology, increased expression of contractile and myofibrogenic proteins, abnormal calcium signaling, lipid peroxidation, oxidative and nitrosative stress, NF-κB activation, and inflammatory signaling. Hypoxic conditions amplified portions of the response. These effects are relevant because COVID-19 can generate precisely the systemic environments in which vascular stress, inflammation, and altered oxygenation interact.
A separate study examined the receptor-binding domain and found that it potentiated cerebral capillary constriction through a pathway involving loss of ACE2 from the pericyte surface, altered angiotensin signaling, and downstream AT1 receptor activity. The investigators also demonstrated the effect in human cortical tissue preparations. Reduced microvascular perfusion would be biologically relevant to fatigue, cognitive slowing, and neurological dysfunction, although these experiments do not establish how frequently that mechanism operates in patients.
The defensible conclusion is narrower: spike can directly alter cells that regulate cerebral microvascular function, and it can do so through pathways with known consequences for tissue perfusion and vascular integrity.
Microglia recognize spike as an inflammatory stimulus
The microglial literature now provides one of the more consistent mechanistic threads in this field. Microglia are resident immune cells of the central nervous system, but their functions extend well beyond antimicrobial defense. They participate in synaptic maintenance, tissue surveillance, repair, cytokine signaling, and the removal or remodeling of synaptic structures. Persistent or dysregulated activation therefore has consequences for neural function.
Frank and colleagues demonstrated that the SARS-CoV-2 S1 subunit could behave in a pathogen-associated-molecular-pattern-like manner, provoking neuroinflammation, microglial activation, and sickness behavior independently of replicating virus. Other investigators showed that S1 increased TNF-α, IL-6, IL-1β, nitric-oxide-associated signaling, NF-κB activation, p38 MAPK signaling, and NLRP3 inflammasome activity in microglial systems.
Experiments using cultured human microglia have added specificity. Full-length recombinant spike stimulated IL-1β, IL-6, CXCL8, and MMP-9 through TLR4-associated signaling, while isolated receptor-binding domain produced a somewhat different inflammatory response associated with ACE2-related signaling. Other work showed that both SARS-CoV-2 and purified spike could prime or activate components of the NLRP3 inflammasome.
These studies should not be interpreted as proof that equivalent protein concentrations occur in human brain tissue after infection. They do demonstrate, however, that the inflammatory effects of spike do not require the complete replicating virus. Spike itself contains biologically active molecular features capable of engaging nervous-system immune cells.
That point matters because microgliosis is not specific to SARS-CoV-2, and spike is certainly not its only cause. The question is whether spike can be one of its causes. The experimental answer is yes.
TLR4, NLRP3, and synaptic architecture
The evidence becomes more consequential when experiments move beyond inflammatory markers and examine structural or behavioral consequences.
A 2023 study directly introduced spike into mouse brain and observed delayed cognitive impairment, hippocampal microgliosis, and complement-dependent synaptic elimination. Blocking TLR4 genetically or pharmacologically prevented both spike-associated synaptic loss and memory dysfunction. The investigators also examined a small human cohort and reported an association between TLR4 genotype and cognitive outcome following COVID-19.
The mechanistic sequence is therefore more specific than “spike causes inflammation.” The experiments support a model in which spike engages TLR4-associated signaling, activates microglia, recruits complement-linked mechanisms of synaptic engulfment, and produces measurable loss of synaptic structure accompanied by impaired memory.
A subsequent Experimental Neurology study strengthened the NLRP3 component. S1 administration produced cognitive impairment, neuronal loss, and neuroinflammation in mice, while both global NLRP3 deletion and microglia-specific NLRP3 deletion attenuated those effects. Pharmacological inhibition of TLR4 also reduced inflammatory signaling in S1-stimulated microglial cells.
Within these experimental systems, that is causal evidence rather than simple correlation. The major uncertainty lies in pharmacokinetic relevance. Direct cerebral administration bypasses several barriers that determine exposure after respiratory infection. Such experiments establish what spike can do once present in neural tissue; they do not establish how much spike reaches equivalent compartments in humans, in what molecular form, or for how long.
That limitation has become less decisive, however, because spike persistence in anatomically relevant human tissues has now been reported.
Persistent spike along the skull-meninges-brain axis
Rong and colleagues reported in Cell Host & Microbe that SARS-CoV-2 spike protein could be detected along the skull-meninges-brain axis in tissue specimens from people who had experienced COVID-19. Their tissue-clearing and imaging studies identified persistence after clearance of acute infection and were accompanied by inflammatory and neurodegeneration-associated proteomic abnormalities. The investigators also reported elevated neurodegeneration-related markers in cerebrospinal fluid from patients with long COVID.
The animal experiments in the same study are particularly important because they attempted to isolate spike from the remainder of the virus. Administration of spike alone produced neuroinflammation and alterations in the tissue proteome, generated anxiety-like behavioral changes, and worsened outcomes following experimental stroke and traumatic brain injury.
This does not establish that persistent spike is the principal cause of long-COVID neurological disease. Detection of a protein does not establish that it remains biologically active at every site where it can be detected, and immunoreactivity does not automatically establish intact structure, concentration-dependent toxicity, or continuing receptor activity. Patients with persistent spike may simultaneously harbor viral RNA, other viral antigens, autoantibodies, endothelial injury, altered coagulation, immune dysregulation, and other abnormalities.
The result nevertheless changes the evidentiary landscape. It is no longer reasonable to treat persistence of spike in anatomically relevant human compartments as merely hypothetical.
The 2026 Kv1.3 finding adds a specific affective pathway
A 2026 study in Biological Psychiatry Global Open Science added a more specific microglial mechanism. Lee and colleagues examined Kv1.3 potassium-channel activity following S1 exposure and found increased Kv1.3 activity and microglial activation within the lateral septum. Exposed mice developed behavioral changes interpreted as anxiety-like and depressive-like phenotypes, and pharmacological inhibition of Kv1.3 attenuated portions of the response.
This finding advances the literature beyond generalized inflammatory signaling. Kv1.3 has a defined role in microglial activation, while the lateral septum participates in stress, affective behavior, and emotional regulation. The investigators therefore linked a viral protein component to a specific ion channel, a defined cellular response, a relevant brain region, and a behavioral phenotype.
The caveat remains the same: experimental S1 administration demonstrates biological capability, not population attributable risk. Human depression and anxiety are far more heterogeneous than rodent behavioral proxies, and translating between the two requires caution.
Astrocytic Cx43 adds another independent mechanism
A second 2026 study, published in Brain, Behavior, and Immunity, identified a different route involving astrocytes rather than microglia. Yuan and colleagues introduced SARS-CoV-2 receptor-binding domain into the medial prefrontal cortex of mice and observed depressive-like behavior, reduced neuronal excitability, and altered functional connectivity. They traced those abnormalities to impaired astrocytic gap-junction communication involving connexin 43, or Cx43.
RBD exposure reduced astrocytic Cx43 expression and disrupted intercellular transfer through gap junctions. Experimental manipulation of Cx43 reproduced or mitigated components of the phenotype, while the investigators also identified increased type I interferon signaling and activation of the cGAS-STING pathway. Restoration of Cx43 function ameliorated the behavioral abnormalities.
This is important because it adds a mechanistically independent route from spike-related exposure to altered neural behavior. The literature no longer rests on a single claim that spike activates inflammatory cytokines. Distinct experimental systems now implicate endothelial cells, pericytes, microglia, complement-mediated synaptic elimination, Kv1.3 signaling, astrocytic gap junctions, and mitochondrial pathways.
Independent mechanisms do not prove human disease causation, but convergence across biological systems strengthens the case that spike is not neurologically inert.
Monoamine metabolism and mitochondrial function
Another potentially important pathway involves monoamine oxidase B, or MAO-B, a mitochondrial enzyme involved in the metabolism of monoamine neurotransmitters.
A 2023 study reported an interaction between SARS-CoV-2 spike glycoprotein and MAO-B in cellular systems. Spike increased MAO-B activity, impaired mitochondrial bioenergetics, increased oxidative stress, and disrupted mitophagy in neuron-like cells. These observations are relevant because mitochondrial dysfunction and altered monoamine metabolism can both affect neural signaling, although the clinical importance of this particular spike-MAO-B interaction remains unresolved.
A 2025 study of post-COVID neuropsychiatric disease provides a separate but complementary line of evidence. Investigators studying people with post-COVID condition found increased inflammatory cytokines, with IL-6 particularly associated with depression. Experimental SARS-CoV-2 infection increased MAO expression and activity in human neural cells and mouse brain tissue. Infected mice developed temporally changing depression- and anxiety-like behaviors, and MAO inhibition reduced those abnormalities.
The second study examined infection rather than isolated spike, so its MAO findings cannot be assigned specifically to spike. Taken together with the spike-MAO-B experiments, however, it identifies a plausible intersection among viral exposure, inflammatory signaling, mitochondrial dysfunction, monoamine metabolism, and behavioral change. That hypothesis now deserves direct human testing.
Serotonin biology demonstrates why a spike-only model would be inadequate
One of the strongest mechanistic studies of long COVID identified a pathway that does not require direct spike toxicity at all.
Wong and colleagues reported reduced peripheral serotonin in post-acute sequelae of viral infection and linked persistent viral material and type I interferon signaling to impaired intestinal tryptophan absorption, altered platelet serotonin storage, and increased monoamine turnover. Reduced peripheral serotonin impaired vagal signaling and hippocampal responses in their experimental system.
This study is especially important because it demonstrates why any comprehensive theory of post-COVID neurological disease must remain multicausal. Persistent viral material can maintain interferon signaling; inflammation can alter tryptophan metabolism; platelet abnormalities can change serotonin handling; autonomic signaling can be disturbed; endothelial function can deteriorate; and coagulation pathways can shift. None of these mechanisms requires direct neuronal toxicity from spike, although several could operate simultaneously with spike-mediated injury.
The scientific error would be to demonstrate that spike is capable of producing neurological injury and then use that observation to absorb every post-COVID symptom into a single “spike toxicity” model. That would replace causal analysis with preferred-hypothesis capture.
“Mental health” is too imprecise a biological endpoint
The methodological weaknesses in this literature are not trivial.
Depression is not cognitive impairment, anxiety is not fatigue, anhedonia is not memory loss, sleep disturbance is not executive dysfunction, and subjective brain fog is not equivalent to an objectively measured neurocognitive deficit. When investigators pool these outcomes under the general heading of “mental health,” they sacrifice biological specificity and make mechanistic inference more difficult.
The two-year analysis by Taquet and colleagues illustrates the problem particularly well. Mood and anxiety outcomes showed temporal trajectories different from those of cognitive and several neurological outcomes. A common exposure may still contribute to several endpoints, but that proposition has to be demonstrated rather than assumed.
Ascertainment bias also deserves attention. Patients with prolonged physical illness interact more frequently with healthcare systems and therefore have more opportunities to acquire psychiatric or neurological diagnoses. Disease severity, pre-existing illness, medication exposure, socioeconomic disruption, intensive-care treatment, and baseline psychiatric status introduce additional confounding. Long-COVID studies also vary substantially in phenotype definition and follow-up interval, while meta-analyses repeatedly report considerable heterogeneity.
These limitations do not erase the observed signal. They define the precision with which the signal can be interpreted.
What the evidence now supports
The evidence currently supports several propositions with reasonable confidence. SARS-CoV-2 infection is associated with subsequent neurological, cognitive, and psychiatric morbidity in humans. Blood-brain-barrier abnormalities have been demonstrated directly in patients with cognitive long COVID. Spike, S1, and RBD can alter endothelial cells, brain pericytes, microglia, and astrocytes in experimental systems. Spike can activate TLR4-, NF-κB-, and NLRP3-associated pathways and can produce microglial responses capable of altering synaptic architecture. Spike-only experimental exposures have generated cognitive abnormalities and anxiety- or depression-like behavior through more than one independently described mechanism. Finally, persistent spike has been detected in human tissues along the skull-meninges-brain axis following infection.
Taken together, these observations make a biologically active role for persistent spike plausible and experimentally supported.
That proposition no longer depends on one cell-culture experiment or one inflammatory biomarker.
What remains unproven
The unanswered questions are equally important. No adequately controlled human study has established a quantitative exposure-response relationship between persistent spike concentration and a defined increase in depression, anxiety, cognitive impairment, or another neuropsychiatric endpoint. No study has established the tissue concentration of spike required to reproduce in humans the effects observed in experimental systems. No accepted clinical assay converts an individual’s circulating or tissue spike measurement into a validated estimate of neurological or psychiatric risk.
Most importantly, no human intervention study has yet shown that selectively reducing persistent spike reverses a defined neuropsychiatric syndrome. Such evidence would be much stronger than an association between persistence and symptoms because it would directly test whether altering the proposed causal exposure alters the predicted outcome.
The field therefore sits at an intermediate stage. It has moved beyond mere speculation, but it has not reached quantitative human causal attribution.
Source, dose, molecular form, compartment, and duration cannot be ignored
The term “spike protein” itself hides important distinctions. Full-length membrane-bound spike is not necessarily biologically equivalent to soluble S1. S1 is not identical to isolated RBD. Endogenously expressed spike may distribute differently from injected recombinant protein. Intracerebral administration is not equivalent to respiratory infection, and acute high-concentration exposure is not equivalent to persistent low-level exposure.
These distinctions are central rather than technical. Biological effects depend upon concentration, molecular conformation, post-translational state, cellular compartment, receptor accessibility, duration of exposure, and the inflammatory environment in which exposure occurs.
Spike generated during replicating infection is also present alongside nucleocapsid and other viral proteins, cellular injury products, interferons, cytokines, damaged endothelium, activated platelets, and potentially persistent viral reservoirs. Evidence obtained from infection therefore cannot automatically be assigned to spike, just as evidence obtained with one recombinant spike construct cannot automatically be generalized to every other form of the protein.
The same rule should govern comparisons among different sources of spike exposure. Molecular design, dose, biodistribution, persistence, and compartment-specific exposure must be measured rather than assumed.
A causal model that can now be tested
The emerging literature supports a network of interacting mechanisms rather than one linear pathway. At the neurovascular interface, persistent or circulating spike may contribute to endothelial or pericyte dysfunction, altered blood-brain-barrier integrity, and impaired cerebral microvascular regulation. Within innate immune pathways, spike can engage TLR4-, NF-κB-, and NLRP3-associated signaling, activating microglia and potentially promoting complement-mediated synaptic remodeling. Kv1.3 activation provides one experimentally defined route connecting S1 exposure with microglial activation in affective circuitry, while astrocytic Cx43 disruption provides a separate mechanism capable of altering intercellular communication, neuronal excitability, and functional connectivity.
At the metabolic level, spike-associated or infection-associated signaling may affect MAO activity, mitochondrial function, oxidative stress, and monoamine metabolism. Independent of direct spike activity, persistent viral material may maintain interferon signaling, alter tryptophan availability and serotonin physiology, disturb vagal signaling, and affect hippocampal function.
These pathways can coexist. That is precisely why observational studies that measure only symptoms cannot determine which pathway dominates in a particular patient.
The study that should come next
The next generation of studies should be prospective, longitudinal, and explicitly mechanistic. Patients should be enrolled following well-characterized SARS-CoV-2 infection and followed with repeated measurements of viral antigens, inflammatory markers, endothelial and coagulation measures, autonomic function, objective neurocognitive testing, and carefully separated psychiatric endpoints.
Where technically feasible, investigators should distinguish full-length spike, soluble S1, RBD-containing fragments, and other SARS-CoV-2 antigens rather than treating “spike” as a unitary exposure. Viral RNA and evidence of replicative persistence should be assessed independently so that persistent spike is not simply used as a surrogate for persistent virus. Mechanistic subcohorts should incorporate blood-brain-barrier imaging, vascular assessments, and, where ethically justified, cerebrospinal-fluid studies.
Baseline psychiatric status must be established rather than reconstructed retrospectively. Depression, anxiety, anhedonia, fatigue, sleep disturbance, memory, attention, and executive function should be analyzed separately. Acute disease severity, treatment exposure, vascular disease, medications, pre-existing neurological illness, and socioeconomic disruption should be measured directly and incorporated into the analysis.
The principal statistical question should be whether persistent spike predicts subsequent neuropsychiatric abnormalities after accounting for viral persistence, systemic inflammation, endothelial injury, baseline neurological and psychiatric health, acute disease severity, medication exposure, and competing mechanistic explanations.
Even a strong prospective association would not by itself settle causality. The most decisive evidence would come from an intervention capable of selectively altering the proposed spike exposure and demonstrating a corresponding change in the predicted downstream biological and clinical phenotype.
That experiment has not yet been completed.
Conclusion
The evidence concerning SARS-CoV-2 spike protein and neurological health has changed substantially since the earliest phase of the pandemic. Spike has demonstrated biological activity at the blood-brain barrier, in cerebral pericytes, in microglia, in astrocytes, in mitochondrial systems, and in pathways involved in synaptic integrity and monoamine metabolism. Spike-only experimental exposures have produced cognitive abnormalities and anxiety- or depression-like behavior in animal models, and persistent spike has been detected in human tissues associated with the skull-meninges-brain axis after infection.
These findings establish mechanistic plausibility backed by experimental evidence. They do not establish that spike explains all, most, or any specified percentage of post-COVID psychiatric disease in humans.
That distinction matters because the evidence now cuts in both directions. Treating spike as biologically irrelevant to post-COVID neurological disease ignores a substantial and increasingly diverse experimental literature. Treating spike as the established cause of long-COVID mental illness ignores the unresolved problems of exposure measurement, molecular form, dose, compartment, persistence, competing mechanisms, and human causal attribution.
A more defensible interpretation is that SARS-CoV-2 spike protein has emerged as a biologically credible contributor to neurological and neuropsychiatric pathology through several experimentally demonstrated mechanisms. How much it contributes in humans, which patients are most susceptible, what exposure thresholds matter, how long biologically active spike persists, and whether removing that exposure improves clinical outcomes remain empirical questions.
Those questions are now sufficiently defined that investigators can stop arguing around them and design studies capable of answering them.
Key Primary Sources
Rong Z, et al. Persistence of spike protein at the skull-meninges-brain axis may contribute to the neurological sequelae of COVID-19. Cell Host Microbe. 2024;32:2112-2130.e10. PMID 39615487. DOI 10.1016/j.chom.2024.11.007.
Greene C, et al. Blood-brain barrier disruption and sustained systemic inflammation in individuals with long COVID-associated cognitive impairment. Nature Neuroscience. 2024;27:421-432. PMID 38388736. DOI 10.1038/s41593-024-01576-9.
DeOre BJ, et al. SARS-CoV-2 Spike Protein Disrupts Blood-Brain Barrier Integrity via RhoA Activation. J Neuroimmune Pharmacol. 2021;16:722-728. PMID 34687399. DOI 10.1007/s11481-021-10029-0.
Khaddaj-Mallat R, et al. SARS-CoV-2 deregulates the vascular and immune functions of brain pericytes via Spike protein. Neurobiology of Disease. 2021;161:105561. PMID 34780863. DOI 10.1016/j.nbd.2021.105561.
Frank MG, et al. SARS-CoV-2 spike S1 subunit induces neuroinflammatory, microglial and behavioral sickness responses: Evidence of PAMP-like properties. Brain Behav Immun. 2022;100:267-277. PMID 34915155. DOI 10.1016/j.bbi.2021.12.007.
Lee H-Y, et al. SARS-CoV-2 Spike Protein S1 Subunit Induces Neuroinflammation Via Microglial Kv1.3 Channel. Biological Psychiatry Global Open Science. 2026;6:100716. PMID 42016325. DOI 10.1016/j.bpsgos.2026.100716.
Yuan R-L, et al. SARS-CoV-2 spike protein induces depressive-like behaviors by disrupting astrocytic Cx43-mediated gap junction intercellular communication. Brain Behav Immun. 2026;131:106176. PMID 41238086. DOI 10.1016/j.bbi.2025.106176.
Wong AC, et al. Serotonin reduction in post-acute sequelae of viral infection. Cell. 2023;186:4851-4867.e20. PMID 37848036. DOI 10.1016/j.cell.2023.09.013.
Taquet M, et al. Neurological and psychiatric risk trajectories after SARS-CoV-2 infection: an analysis of 2-year retrospective cohort studies including 1,284,437 patients. Lancet Psychiatry. 2022;9:815-827. PMID 35987197. DOI 10.1016/S2215-0366(22)00260-7.
IPAK-EDU is grateful to Popular Rationalism as this piece was originally published there and is included in this news feed with mutual agreement. Read More
Leave a Reply