Dementia and COVID-19, a Bidirectional Liaison: Risk Factors, Biomarkers, and Optimal Health Care

Abstract

Cognitive impairment following SARS-CoV-2 infection is being increasingly recognized as an acute and possibly also long-term sequela of the disease. Direct viral entry as well as systemic mechanisms such as cytokine storm are thought to contribute to neuroinflammation in these patients. Biomarkers of COVID-19-induced cognitive impairment are currently lacking, but there is some limited evidence that SARS-CoV-2 could preferentially target the frontal lobes, as suggested by behavioral and dysexecutive symptoms, fronto-temporal hypoperfusion on MRI, EEG slowing in frontal regions, and frontal hypometabolism on 18F-FDG-PET. Possible confounders include cognitive impairment due to hypoxia and mechanical ventilation and post-traumatic stress disorder. Conversely, patients already suffering from dementia, as well as their caregivers, have been greatly impacted by the disruption of their care caused by COVID-19. Patients with dementia have experienced worsening of cognitive, behavioral, and psychological symptoms, and the rate of COVID-19-related deaths is disproportionately high among cognitively impaired people. Multiple factors, such as difficulties in remembering and executing safeguarding procedures, age, comorbidities, residing in care homes, and poorer access to hospital standard of care play a role in the increased morbidity and mortality. Non-pharmacological interventions and new technologies have shown a potential for the management of patients with dementia, and for the support of their caregivers.

Metabolic correlates of olfactory dysfunction in COVID-19 and Parkinson’s disease (PD) do not overlap

“…Indeed, during the last year, the scientific community has paid great attention to the risk and predictors of neurological sequelae of COVID-19 [ 1 , 37 ]. As hyposmia is also e feature a of prodromal PD and of other neurodegenerative diseases and given the fact that that parkinsonism has been reported in few patients following COVID-19, a hypothetical link between SARS-CoV-2 infection and PD has been previously proposed [ 23 ].…”

Monoclonal Human Antibodies That Recognise the Exposed N and C Terminal Regions of the Often-Overlooked SARS-CoV-2 ORF3a Transmembrane Protein

“…In those regions of the world claiming a level of pandemic-control, a new and growing epidemic of patients suffering from longer-term post-infection complications, often referred to by the catch-all "long-COVID", is being increasingly reported. Whilst long-COVID is a condition that is still not well understood, there are some pointers in the general condition that suggest that inflammation responses, linked to long term viral infection, may be at its core, with various tissues and even different organs affected [37,[56][57][58][59].…”

Relationship Between Coronavirus Disease 2019 and Alzheimer’s Disease

“…Published literature has also found a potential link that cognitive impairment following SARS-CoV-2 infection is being increasingly recognized as an acute and possibly also longterm sequelae of the disease [28]. Researchers have found in patients suffering neurological sequelae of the disease a direct viral invasion through infected vascular endothelial cells directly to glial cells has also been described, as well as penetrance from the olfactory epithelium to the olfactory bulb through retrograde axonal transport along the olfactory nerve [29].…”

“…Researchers have found in patients suffering neurological sequelae of the disease a direct viral invasion through infected vascular endothelial cells directly to glial cells has also been described, as well as penetrance from the olfactory epithelium to the olfactory bulb through retrograde axonal transport along the olfactory nerve [29]. It has also been discovered that there is some limited evidence that SARS-CoV-2 could preferentially target the frontal lobes, as suggested by behavioral and dysexecutive symptoms, fronto-temporal hypoperfusion on MRI, EEG slowing in frontal regions, and frontal hypometabolism on 18F-FDG-PET [28]. 320 Fascinatingly, immune responses and excessive inflammation in Covid 19 may also accelerate the progression of brain inflammatory neurodegeneration [30].…”

“…Direct viral invasion through infected vascular endothelial cells directly to glial cells has also been described, as well as penetrance from the olfactory epithelium to the 317 olfactory bulb through retrograde axonal transport along the olfactory nerve in patients suffering neurological sequelae of the disease [29]. Biomarkers of Covid 19 induced cognitive impairment are currently lacking, but there is some limited evidence that SARS-CoV-2 could preferentially target the frontal lobes, as suggested by behavioral and dysexecutive symptoms, fronto-temporal hypoperfusion on MRI, EEG slowing in frontal regions, and frontal hypometabolism on 18F-FDG-PET [28].…”