CROI 2024 Abstract eBook

Abstract eBook

Poster Abstracts

3D ASL sequence was used (TA: 4:59, voxel: 1.5×1.5×3.0 mmRel, SNR: 1.00, TR: 4600ms, TE: 16.18ms). Post-processing was completed using MATLAB and the Harvard-Oxford atlas to generate CBF for 48 cortical and 21 subcortical regions of interest (ROI). Group comparisons used non-parametric statistics. Results: 14 participants with cognitive N-PASC (median age 43 [IQR 37 – 55], 79% female, median 450 days after COVID-19 symptom onset [IQR 354 – 694]) and 6 controls (median age 34 [30 – 40], 67% female) underwent MRI. The groups did not differ in age, gender, race, or cardiovascular risk factors, which were low in prevalence. CBF was lower in N-PASC compared to controls (C) in the right supplementary motor area (N-PASC: median of 22.5 mL/g/min and C: 27.7 mL/g/min; p = 0.025). a trend of hypoperfusion that did not reach significance was identified in three other ROIs in the right hemisphere: the frontal pole (N-PASC: 23.5 mL/g/min and C: 30.4 mL/g/min; p = 0.06), middle frontal gyrus (N-PASC: 24.8 mL/g/min and C: 31.3 mL/g/min; p = 0.06), and post-central gyrus (N-PASC: 22.5 mL/g/min and C: 27.7 mL/g/min; p = 0.06). There was no difference in CBF between groups in the remaining ROIs. Conclusion: We report preliminary evidence of focal hypoperfusion in the right frontal lobe and a trend of hypoperfusion in the right parietal lobe in individuals with N-PASC. These findings suggest that altered perfusion in the non-dominant hemisphere may play a role in cognitive N-PASC symptoms, possibly by affecting motor speed and motor control of speech. We look forward to collecting additional data to investigate the mechanism of decreased cortical perfusion in cognitive N-PASC. CSF Biomarker Evidence of Synaptic Dysfunction in Acute, but Not Post-Acute COVID-19 Arvid Edén , Johanna Nilsson, Anna Grahn, Nelly Kanberg, Erika Stentoft, Daniel Bremell, Aylin Yilmaz, Marie Studahl, Staffan Nilsson, Michael Schöll, Iris Bosch, Kaj Blennow, Ann Brinkmalm, Henrik Zetterberg, Magnus Gisslén Sahlgrenska Academy at the University of Gothenburg, Gothenburg, Sweden Background: CNS immune activation and neurocognitive symptoms are common in severe COVID-19, but mechanisms of persisting CNS dysfunction in post COVID-19 conditions (PCC; "long covid") are unclear. We used a panel of CSF markers, several of whom have been implicated in Alzheimer's disease (AD) and other neurodegenerative diseases to investigate synaptic and lysosomal dysfunction in acute and post-acute COVID-19. Methods: Lumbar punctures were performed on 76 (49 male) patients and 20 (6 male) healthy controls from longitudinal studies, sampled during acute (46), ≥3 (39 [31 PCC]) and/or ≥12 (25 [19 PCC]) months after COVID-19. PCC symptoms at follow-up were evaluated by interview and self-report. The 37-marker CSF panel included cathepsins, calsyntenins, contactins, granins, glutamate receptor 4 (GRIA4), VGF, APP, neurogranin, syntaxins, LAMPs, beta-hexosaminidase subunit beta (HEXB), GM2A, dipeptidyl peptidase 2 (DPP-2), NCAM2, NSF, synapsin-1, CAMK2A, Thy-1, VAMP2, AP2B1, complexins, synucleins, GDI-1, neuronal pentraxins, PEBP-1, and members of the 14-3-3 protein family. A micro-high performance liquid chromatography mass spectrometry system (6495 Triple Quadrupole LC/MS system, Agilent Technologies) equipped with a Hypersil Gold reversed-phase C18 column (dim.=100 × 2.1 mm, particle size=1.9 μm, Thermo Fisher Scientific) was used for quantitation. Group comparisons of biomarker concentrations were analyzed by Kruskal-Wallis (Dunn's post hoc) test. Results: Patients had mild (15), moderate (hospitalized with oxygen; 33) or severe (ICU; 28) COVID-19. Self-reported PCC symptom severity was mild or moderate. Significant alterations of GRIA4, DPP-2, cathepsin F, HEXB (all decreased) and 14-3-3 zeta/delta (increased), were seen in acute compared with post-acute COVID-19 and controls (all p<0.005 [Figure 1]). No significant differences in any biomarkers were seen between patients and controls, or between patients with PCC compared with fully recovered patients ≥3 or ≥12 months after acute infection.

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The Association Between Prior SARS-CoV-2 Infection and Incidence of Stroke Naveed Akhtar 1 , Hiam Chemaitelly 2 , Saadat Kamran 1 , Abdul-Badi Abou-Samra 1 , Laith J. Abu-Raddad 2 , Adeel A Butt 1 1 Hamad Medical Corporation, Doha, Qatar, 2 Weill Cornell Medicine College in Qatar, Doha, Qatar Background: Individuals with COVID-19 have an increased incidence of several comorbid conditions including diabetes and acute myocardial infarction. The association of COVID-19 infection with stroke is controversial, with some studies demonstrating a higher risk and other studies showing no association or even a protective effect. We sought to determine the association between COVID-19 infection and subsequent incidence of stroke at a national level in Qatar. Methods: We used the Qatar Stroke Database to identify individuals who were admitted with acute ischemic or hemorrhagic stroke to the tertiary care referral hospital in Qatar, which accounts for 98% of all acute stroke admissions in Qatar. For the current study, we included individuals admitted with acute stroke between March 1, 2020 and April 11, 2023. We linked the Qatar Stroke Database to the Qatar National COVID-19 database to retrieve the information on COVID-19 testing and vaccination. This database contains all records of RT-PCR and medically-supervised antigen testing and vaccination in the State of Qatar. Eligible individuals with stroke diagnosis were exactly matched 1:1 on 10-year age group, sex, nationality, type of comorbid condition, and number of vaccine doses received, to eligible controls who tested SARS-CoV-2-negative during the same week of the stroke diagnosis. We utilized a case-control design to determine the association of COVID-19 diagnosis with acute stroke. Adjusted odds ratios and corresponding 95% confidence intervals were calculated for the entire study population and subgroups by age, nationality, and prior infection variant period (infection in the pre-omicron era, omicron era, or in both eras). Results: A total of 1,640 matched pairs were analyzed. Median age was 49 years, 85% were male, 11% were Qatari nationals, 58% had no comorbidities, and 48% were unvaccinated at the time of first stroke diagnosis. Any prior infection was associated with a lower risk of stroke (aOR 0.48, 95% CI 0.40,0.58). The protective association was consistent across older age groups, among unvaccinated and vaccinated, the infection era (pre-Omicron or Omicron eras) and regardless of the time from infection. (Table) Conclusion: Prior COVID-19 infection is associated with a lower risk of stroke. This association is independent of age, vaccination status, infection era by predominant COVID-19 variant, and time from infection. The reason for this effect is unclear and requires further investigation. The figure, table, or graphic for this abstract has been removed. Focal Cerebral Hypoperfusion in Individuals With Cognitive Impairment After COVID-19 Lindsay S McAlpine , Allison Nelson , Jennifer Chiarella, Robert Fulbright, Shelli Farhadian, Maolin Qiu, Todd Constable, Serena Spudich Yale University, New Haven, CT, USA Background: Cognitive impairment is a common symptom of neuropsychiatric post-acute sequelae of COVID-19 (N-PASC), characterized by neuropsychological deficits including impaired executive functioning, processing speed, motor speed, attention, recall, and verbal fluency. Little is known about the underlying mechanism of cognitive N-PASC. We report preliminary analyses of noninvasive MRI measurements of brain perfusion in individuals with and without N-PASC. Methods: Participants with cognitive N-PASC (self-reported symptoms of cognitive impairment >3 months after COVID-19) referred from a NeuroCOVID Clinic and controls with prior COVID without PASC underwent an MRI protocol, which included Arterial Spin Labeling (ASL) to assess perfusion (Cerebral Blood Flow; CBF). All imaging was performed on a Siemens 3T MRI scanner. A standard

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CROI 2024 152