2. Academic Validation
  3. Cortical-blood vessel assembloids exhibit Alzheimer's disease phenotypes by activating glia after SARS-CoV-2 infection

Cortical-blood vessel assembloids exhibit Alzheimer's disease phenotypes by activating glia after SARS-CoV-2 infection

  • Cell Death Discov. 2023 Jan 25;9(1):32. doi: 10.1038/s41420-022-01288-8.
Dasom Kong # 1,  Ki Hoon Park # 2,  Da-Hyun Kim 1,  Nam Gyo Kim 1,  Seung-Eun Lee 1,  Nari Shin 1,  Myung Geun Kook 1,  Young Bong Kim 3,  Kyung-Sun Kang 4
Affiliations

Affiliations

  • 1 Adult Stem Cell Research Center and Research Institute for Veterinary Science, College of Veterinary Medicine, Seoul National University, Seoul, 08826, Republic of Korea.
  • 2 Department of Research and Development, KR BIOTECH CO., Ltd., Seoul, 05029, Republic of Korea.
  • 3 Department of Biomedical Science and Engineering, Konkuk Institute of Science and Technology, Konkuk University, Seoul, 05029, Republic of Korea. kimera@konkuk.ac.kr.
  • 4 Adult Stem Cell Research Center and Research Institute for Veterinary Science, College of Veterinary Medicine, Seoul National University, Seoul, 08826, Republic of Korea. kangpub@snu.ac.kr.
  • # Contributed equally.
PMID: 36697403 DOI: 10.1038/s41420-022-01288-8
Abstract

A correlation between COVID-19 and Alzheimer's disease (AD) has been proposed recently. Although the number of case reports on neuroinflammation in COVID-19 patients has increased, studies of SARS-CoV-2 neurotrophic pathology using brain organoids have restricted recapitulation of those phenotypes due to insufficiency of immune cells and absence of vasculature. Cerebral pericytes and endothelial cells, the major components of blood-brain barrier, express viral entry receptors for SARS-CoV-2 and response to systemic inflammation including direct cell death. To overcome the limitations, we developed cortical-blood vessel assembloids by fusing cortical Organoid with blood vessel Organoid to provide vasculature to brain organoids a nd obtained the characteristics of increased expression of microglia and astrocytes in brain organoids. Furthermore, we observed AD pathologies, including β-amyloid plaques, which were affected by the inflammatory response from SARS-CoV-2 Infection. These findings provide an advanced platform to investigate human neurotrophic diseases, including COVID-19, and suggest that neuroinflammation caused by viral Infection facilitates AD pathology.

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