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Cognitive Dysfunction in Long COVID
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This entry is adapted from: 10.3390/ijms26115102

Cognitive dysfunction in Long COVID refers to the persistence of neurocognitive symptoms such as memory deficits, attention impairment, executive dysfunction, and slowed information processing that continue for weeks or months after acute SARS-CoV-2 infection. These symptoms, commonly termed “brain fog,” are among the most disabling features of post-acute sequelae of COVID-19 (PASC) and occur even in individuals with mild initial disease. The underlying mechanisms involve chronic neuroinflammation, blood–brain barrier disruption, endothelial dysfunction, and neuroendocrine imbalance.

Long Covid Cognitive Dysfunction

1. Introduction

Cognitive dysfunction is one of the most common and debilitating features of Long COVID, a syndrome that affects individuals for weeks or months after recovering from acute SARS-CoV-2 infection. Patients often describe their symptoms as “brain fog,” encompassing difficulties with memory, attention, executive function, and mental clarity. These impairments can occur even in individuals who experienced mild or asymptomatic COVID-19 and may persist long after respiratory symptoms resolve [1][2][3].

The underlying mechanisms of Long COVID-related cognitive impairment remain incompletely understood but appear to involve a convergence of neuroinflammatory, vascular, metabolic, and neuroendocrine pathways. This entry synthesizes current evidence on the molecular and cellular mechanisms implicated in post-COVID cognitive dysfunction.

2. Clinical and Neuropsychological Profile

Cognitive symptoms in Long COVID range from subtle attention deficits to severe executive dysfunction and memory loss. Objective testing using validated tools such as the Montreal Cognitive Assessment (MoCA), Mini-Mental State Examination (MMSE), and Symbol Digit Modalities Test (SDMT) has revealed persistent deficits months after infection [4][5][6]. Meta-analyses suggest that up to 25% of individuals report cognitive symptoms 3–12 months post-infection [7][8], with longitudinal studies confirming worsening or persistence over time [9].

In addition to cognitive symptoms, patients often experience neuropsychiatric manifestations such as depression, anxiety, irritability, and insomnia. However, studies indicate that cognitive deficits often persist independently of mood disorders, supporting a distinct neurobiological substrate [10][11].

3. Neuroinflammation and Glial Activation

Neuroinflammation is a central mechanism in Long COVID cognitive dysfunction. SARS-CoV-2 infection triggers a systemic cytokine response that can extend to the CNS via a compromised blood–brain barrier (BBB) or direct viral neuroinvasion. The release of proinflammatory cytokines, including IL-6, TNF-α, and IL-1β, activates microglial cells, leading to chronic low-grade inflammation within the brain [12][13].

Microglial activation promotes synaptic pruning, oxidative stress, and the release of neurotoxic substances such as nitric oxide and reactive oxygen species (ROS). Astrocytes contribute further to this neurotoxicity by releasing glutamate and cytokines, exacerbating neuronal dysfunction [14][15]. The NLRP3 inflammasome, an intracellular complex, plays a key role in amplifying inflammation by activating caspase-1 and promoting the release of IL-1β and IL-18 [13][16].

4. Blood–Brain Barrier Disruption and Endothelial Dysfunction

The BBB is a highly selective interface between the peripheral circulation and the CNS. Disruption of the BBB during and after SARS-CoV-2 infection allows peripheral immune cells, cytokines, and neurotoxins to infiltrate the CNS, promoting inflammation and neuronal injury [17][18]. The virus can directly infect endothelial cells via ACE2 and neuropilin-1 (NRP1) receptors, disrupting VEGF-A–mediated signaling and promoting vascular permeability [19][20][21][22].

BBB disruption has been confirmed in imaging and cerebrospinal fluid (CSF) studies in Long COVID patients, with findings including elevated S100B, increased albumin index, and radiological evidence of microvascular pathology [18][23]. These abnormalities correlate with neurocognitive symptoms and glial markers such as GFAP and NFL.

5. Cerebral Microvascular Injury and Thrombosis

SARS-CoV-2-induced endothelial injury contributes to cerebral microvascular thrombosis and impaired cerebral perfusion. Endothelial cells express adhesion molecules (ICAM-1, VCAM-1) that promote leukocyte adhesion and platelet aggregation. This pro-thrombotic state leads to microclots, particularly in metabolically active brain regions like the hippocampus and prefrontal cortex [24][25][26].

Persistent hypercoagulability has been documented in Long COVID, with elevated D-dimer and fibrinogen levels months after infection. These microvascular alterations may not be visible on conventional MRI but are associated with ischemia, mitochondrial fragmentation, and neuronal apoptosis [27][28].

6. Neuroendocrine Dysregulation and Autonomic Dysfunction

Long COVID is also characterized by alterations in the hypothalamic–pituitary–adrenal (HPA) axis and autonomic nervous system (ANS). Patients frequently exhibit hypocortisolism, suggesting central suppression of HPA function, which may result from hypothalamic inflammation or impaired pituitary feedback [29][30][31][32]. Low cortisol levels contribute to fatigue, mood changes, and cognitive decline [33].

Dysautonomia, including postural orthostatic tachycardia syndrome (POTS), orthostatic intolerance, and palpitations, has been widely reported [34][35]. Reduced vagal tone impairs the cholinergic anti-inflammatory reflex, exacerbating systemic inflammation and cognitive symptoms. Heart rate variability (HRV) has emerged as a surrogate marker of vagal activity and a predictor of cognitive risk in Long COVID [36][37].

7. Molecular Signatures and Biomarkers

Several molecular biomarkers have been associated with Long COVID cognitive dysfunction:

- Cytokines: IL-6, IL-1β, TNF-α [12][16][38]
- Glial injury markers: GFAP, LGALS3 (galectin-3), S100B [39][12][40][18]
- Axonal damage: NFL (neurofilament light chain) [11][41]
- MicroRNAs: miR-146a and miR-155 modulate NF-κB signaling and glial reactivity; miR-24 regulates BBB integrity via NRP1 suppression [12][42][43]
- Endothelial markers: ICAM-1, VCAM-1, VEGF-A [18][23]
- Neuroendocrine markers: Cortisol, serotonin, dopamine [44][45][29]

These biomarkers are useful for identifying disease severity, monitoring recovery, and guiding treatment strategies.

8. Overlap with Neurodegenerative Disorders

Long COVID exhibits striking pathophysiological parallels with Alzheimer’s disease (AD), including chronic neuroinflammation, tau hyperphosphorylation, mitochondrial dysfunction, and BBB disruption [12][40][46]. Transcriptomic analyses show upregulation of genes such as FKBP5, LGALS3, and KLF4 in both conditions, indicating overlapping neurodegenerative cascades [47][48].

Experimental models have confirmed that SARS-CoV-2 can induce astrogliosis, tauopathy, and hippocampal neurogenesis suppression, even in the absence of viral RNA in brain tissue [49][50][51]. These findings suggest that Long COVID may accelerate neurodegenerative processes, particularly in genetically predisposed individuals (e.g., APOE ε4 carriers) [52][53].

9. Therapeutic Strategies

Several therapeutic strategies are under investigation:

- Anti-cytokine therapies: IL-6 receptor antagonists (e.g., tocilizumab) and TNF-α inhibitors (e.g., infliximab) may reduce neuroinflammation [54][55].
- Antioxidant and neuroprotective compounds: Nutraceuticals such as resveratrol, curcumin, and green tea polyphenols activate NRF2, PPARγ, and AMPK signaling, improving mitochondrial function and reducing oxidative stress [56][48][57][50][58].
- Supportive therapies: Cortisol supplementation and magnesium correction may alleviate neuroendocrine dysfunction and improve fatigue and cognition [29][59].

Targeting the NRF2/PPARγ–NF-κB axis may represent a dual-acting strategy to suppress glial activation and enhance resilience to oxidative damage.

10. Conclusion

Cognitive dysfunction in Long COVID is driven by a multifaceted interplay of neuroinflammation, BBB and vascular injury, endothelial dysfunction, and neuroendocrine imbalance. These processes are reflected in specific molecular profiles, many of which overlap with known neurodegenerative conditions. The identification of biomarkers such as IL-6, TNF-α, GFAP, NFL, and miR-146a offers new tools for diagnosis and stratification.

Future research should focus on longitudinal biomarker profiling, advanced neuroimaging, and mechanistic studies to clarify disease trajectories and identify effective interventions. Integrative, personalized approaches will be essential for managing and potentially reversing cognitive impairment in Long COVID.

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