tetano
Editor, Senior Moderator
Acta Neuropathol
. 2024 May 27;147(1):92.
doi: 10.1007/s00401-024-02743-9. Neuropathological findings in Down syndrome, Alzheimer's disease and control patients with and without SARS-COV-2: preliminary findings
Ann-Charlotte E Granholm[SUP] 1 [/SUP], Elisabet Englund[SUP] 2 [/SUP], Anah Gilmore[SUP] 3 [/SUP], Elizabeth Head[SUP] 4 5 [/SUP], William H Yong[SUP] 4 [/SUP], Sylvia E Perez[SUP] 6 [/SUP], Samuel J Guzman[SUP] 7 [/SUP], Eric D Hamlett[SUP] 8 [/SUP], Elliott J Mufson[SUP] 6 [/SUP]
Affiliations
The SARS-CoV-2 virus that led to COVID-19 is associated with significant and long-lasting neurologic symptoms in many patients, with an increased mortality risk for people with Alzheimer's disease (AD) and/or Down syndrome (DS). However, few studies have evaluated the neuropathological and inflammatory sequelae in postmortem brain tissue obtained from AD and people with DS with severe SARS-CoV-2 infections. We examined tau, beta-amyloid (Aβ), inflammatory markers and SARS-CoV-2 nucleoprotein in DS, AD, and healthy non-demented controls with COVID-19 and compared with non-infected brain tissue from each disease group (total n = 24). A nested ANOVA was used to determine regional effects of the COVID-19 infection on arborization of astrocytes (Sholl analysis) and percent-stained area of Iba-1 and TMEM 119. SARS-CoV-2 antibodies labeled neurons and glial cells in the frontal cortex of all subjects with COVID-19, and in the hippocampus of two of the three DS COVID-19 cases. SARS-CoV-2-related alterations were observed in peri-vascular astrocytes and microglial cells in the gray matter of the frontal cortex, hippocampus, and para-hippocampal gyrus. Bright field microscopy revealed scattered intracellular and diffuse extracellular Aβ deposits in the hippocampus of controls with confirmed SARS-CoV-2 infections. Overall, the present preliminary findings suggest that SARS-CoV-2 infections induce abnormal inflammatory responses in Down syndrome.
Keywords: Alzheimer’s disease; Brain; COVID-19; Corona viruses; Down syndrome; Glial cells; Neurologic symptoms; SARS-CoV-2.
. 2024 May 27;147(1):92.
doi: 10.1007/s00401-024-02743-9. Neuropathological findings in Down syndrome, Alzheimer's disease and control patients with and without SARS-COV-2: preliminary findings
Ann-Charlotte E Granholm[SUP] 1 [/SUP], Elisabet Englund[SUP] 2 [/SUP], Anah Gilmore[SUP] 3 [/SUP], Elizabeth Head[SUP] 4 5 [/SUP], William H Yong[SUP] 4 [/SUP], Sylvia E Perez[SUP] 6 [/SUP], Samuel J Guzman[SUP] 7 [/SUP], Eric D Hamlett[SUP] 8 [/SUP], Elliott J Mufson[SUP] 6 [/SUP]
Affiliations
- PMID: 38801558
- DOI: 10.1007/s00401-024-02743-9
The SARS-CoV-2 virus that led to COVID-19 is associated with significant and long-lasting neurologic symptoms in many patients, with an increased mortality risk for people with Alzheimer's disease (AD) and/or Down syndrome (DS). However, few studies have evaluated the neuropathological and inflammatory sequelae in postmortem brain tissue obtained from AD and people with DS with severe SARS-CoV-2 infections. We examined tau, beta-amyloid (Aβ), inflammatory markers and SARS-CoV-2 nucleoprotein in DS, AD, and healthy non-demented controls with COVID-19 and compared with non-infected brain tissue from each disease group (total n = 24). A nested ANOVA was used to determine regional effects of the COVID-19 infection on arborization of astrocytes (Sholl analysis) and percent-stained area of Iba-1 and TMEM 119. SARS-CoV-2 antibodies labeled neurons and glial cells in the frontal cortex of all subjects with COVID-19, and in the hippocampus of two of the three DS COVID-19 cases. SARS-CoV-2-related alterations were observed in peri-vascular astrocytes and microglial cells in the gray matter of the frontal cortex, hippocampus, and para-hippocampal gyrus. Bright field microscopy revealed scattered intracellular and diffuse extracellular Aβ deposits in the hippocampus of controls with confirmed SARS-CoV-2 infections. Overall, the present preliminary findings suggest that SARS-CoV-2 infections induce abnormal inflammatory responses in Down syndrome.
Keywords: Alzheimer’s disease; Brain; COVID-19; Corona viruses; Down syndrome; Glial cells; Neurologic symptoms; SARS-CoV-2.