Inflaming the Brain

Exactly how cerebrovascular alterations contribute to Alzheimer's disease (AD) is still unknown. Merlini et al. (2019) show that blood-derived fibrinogen leads to dendritic spine elimination and cognitive deficit via microglial CD11b/CD18. Fibrinogen may be a significant contributor to AD patho...

Full description

Saved in:
Bibliographic Details
Published inNeuron (Cambridge, Mass.) Vol. 101; no. 6; pp. 991 - 993
Main Authors Ahn, Hyung Jin, Baker, Sarah K., Norris, Erin H., Strickland, Sidney
Format Journal Article
LanguageEnglish
Published United States Elsevier Inc 20.03.2019
Elsevier Limited
Subjects
Alzheimer's disease
Animal cognition
Binding sites
Blood
Brain
CD11b antigen
CD18 antigen
Cognitive ability
Dendritic spines
Disease
Fibrinogen
Genomes
Neurodegenerative diseases
Pathogenesis
Pathology
Online AccessGet full text

Cover

More Information
Summary:Exactly how cerebrovascular alterations contribute to Alzheimer's disease (AD) is still unknown. Merlini et al. (2019) show that blood-derived fibrinogen leads to dendritic spine elimination and cognitive deficit via microglial CD11b/CD18. Fibrinogen may be a significant contributor to AD pathogenesis. Exactly how cerebrovascular alterations contribute to Alzheimer's disease (AD) is still unknown. Merlini et al. (2019) show that blood-derived fibrinogen leads to dendritic spine elimination and cognitive deficit via microglial CD11b/CD18. Fibrinogen may be a significant contributor to AD pathogenesis.
Bibliography:ObjectType-Article-2
SourceType-Scholarly Journals-1
ObjectType-Feature-3
content type line 23
ObjectType-Commentary-1
ISSN:0896-6273
1097-4199
DOI:10.1016/j.neuron.2019.03.007