Therapeutic Intervention of Neuroinflammatory Alzheimer Disease Model by Inhibition of Classical Complement Pathway with the Use of Anti-C1r Loaded Exosomes.
Complement inhibitors
exosome
neuroinflammation
Journal
Research square
Titre abrégé: Res Sq
Pays: United States
ID NLM: 101768035
Informations de publication
Date de publication:
18 Oct 2023
18 Oct 2023
Historique:
pubmed:
27
10
2023
medline:
27
10
2023
entrez:
27
10
2023
Statut:
epublish
Résumé
Alzheimer's disease (AD) is a complex neurodegenerative disease associated with memory decline, cognitive impairment, amyloid plaque formation and tau tangles. Neuroinflammation has been shown to be a precursor to apparent amyloid plaque accumulation and subsequent synaptic loss and cognitive decline. In this study, the ability of a novel, small molecule, T-ALZ01, to inhibit neuroinflammatory processes was analyzed. T-ALZ01, an inhibitor of complement component C1r, demonstrated a significant reduction in the levels of the inflammatory cytokines, IL-6 and TNF-α
Identifiants
pubmed: 37886595
doi: 10.21203/rs.3.rs-3399248/v1
pmc: PMC10602145
pii:
doi:
Types de publication
Preprint
Langues
eng
Déclaration de conflit d'intérêts
Competing interests The authors declare no competing interests.
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