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Table 1 Pathophysiological processes contributing to increased risk of chronic neurological disease, including dementia, in COVID-19 patients

From: Cognitive impact of COVID-19: looking beyond the short term

1. Hypoxia and cerebral hypoperfusion secondary to cardiorespiratory disease [25, 26]
 - Hypoxic-ischaemic brain injury, diffuse white matter damage  
2. Coagulopathy, with thrombotic occlusion of cerebral blood vessels [22]
 - Cerebral artery thrombosis, disseminated intravascular coagulation  
3. Cerebral microvascular damage and dysfunction [23, 24]
 - Endotheliitis, pericyte damage, BBB leakiness, neurovascular dysfunction, impaired autoregulation, impaired vascular/para-vascular drainage  
4. Dysregulation of renin-angiotensin system [125,126,127, 160, 161]
 - Loss of regulatory RAS and overactivity of classical RAS signalling  
5. SARS-CoV-2 encephalitis / post-infective encephalitis (rare) [27, 28, 38], reviewed in [5]
 - CNS viral neuroinvasion via olfactory nerve fibres or vasculature/post-infective immune injury to CNS