Serum and CSF alpha-synuclein levels do not change in COVID-19 patients with neurological symptoms.

SARS-CoV-2 infection can associate diverse neurological manifestations. Several studies have provided proof to support the theory of neurotropic involvement of SARS-CoV-2. Alpha-synuclein has been described as a native antiviral factor within neurons, and upregulation of this protein can be seen in animals that suffered other neuroinvasive infections. To assess if increased expression of this protein takes place in COVID-19 patients with neurological symptoms, we analyzed serum total alpha-synuclein levels in three groups: seven COVID-19 patients with myoclonus, Parkinsonism and/or encephalopathy; thirteen age- and sex-matched COVID-19 patients without neurological involvement and eight age- and sex-matched healthy controls. We did not find differences among them. In a subset of four patients, the change in serum alpha-synuclein before and after the onset of neurological symptoms was not significant either. Cerebrospinal fluid alpha-synuclein levels were also similar between neurological COVID-19 and healthy controls. Overall, these results cannot support the hypothesis of alpha-synuclein upregulation in humans with neurological symptoms in COVID-19. Further research taking into account a larger group of COVID-19 patients including the whole spectrum of neurological manifestations and disease severity is needed.

COVID-19 related mortality in patients with cognitive impairment: A Hospital-based retrospective cohort study

Objective: to analyse the frequency of cognitive impairment and other neurological comorbidities in deceased COVID-19 patients, during the outbreak of the pandemic in Madrid, Spain. Methods: retrospective, single-center, hospital-based study. We included adults that died after admission from March 1 to March 31, 2020, at Hospital Universitario 12 De Octubre. Clinical and demographic data were extracted from electronic medical records. Results: 477 cases: 58 with probable COVID-19, 281 confirmed COVID-19, and 138 who died of other causes. Comparing the latter two groups, median age (81.4 years vs. 78.1 years;p<0.01) and the proportion of males (62.3% vs. 49.3%, p<0.01) were higher in the confirmed COVID-19 group. The number of comorbidities was high and similar in both groups, and cognitive impairment was common (29.9%;21.1% dementia;8.9% mild cognitive impairment) in confirmed COVID-19. In this group group, subjects with cognitive impairment were older (median 85.8 years vs. 79.0 years, p<0.0001), more lived in nursing homes and had slightly shorter times from symptom onset to death than those without cognitive impairment. COVID-19 patients with cognitive impairment were rarely admitted to the ICU, and fewer received non-invasive mechanical ventilation (7.1% vs. 25.4%, <0.0001). Palliative care was provided in more subjects with cognitive impairment (79.2% vs. 66.3%, p=0.038). Conclusions: in our study, dead patients with confirmed COVID-19 were older and had more comorbidities than those reported in the Asian population. Cognitive impairment is a frequent comorbidity in COVID-19 deceased patients. The burden of COVID-19 in the dementia community will be high.