The synthesis of a Tentagel-supported peptide incorporating the reactive triad of serine, histidine and aspartic acid, found within serine protease enzymes, is described.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1039/b302239k | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Background: Microglial activation is an early phenomenon in Alzheimer's disease (AD) that may occur prior to and independently of amyloid-β (Aβ) aggregation. Compelling experimental evidence suggests that the apolipoprotein E ε4 (APOEε4) allele may be a culprit of early microglial activation in AD. However, it is unclear whether the APOEε4 genotype is associated with microglial reactivity in the living human brain.
View Article and Find Full Text PDFBiomarkers.
Alzheimers Dement
December 2024
Translational Neuroimaging Laboratory, The McGill University Research Centre for Studies in Aging, Montréal, QC, Canada.
Background: It has been proposed that microglia release of proinflammatory factors reactive to amyloid plaques constitutes an early event leading to tau pathology. Here, we assessed how the rate of progression of tau-PET and the rate of change in plasma pTau217 are affected by baseline levels of amyloid-β and neuroinflammation.
Methods: We included 93 individuals from TRIAD cohort: 11 young individuals, 57 cognitively unimpaired elderlies, 15 with mild cognitive impairment and 10 individuals with Alzheimer's Disease.
Biomarkers.
Alzheimers Dement
December 2024
Universidade Federal do Rio Grande do Sul, Porto Alegre, Brazil.
Background: Glial reactivity is a key phenomenon in Alzheimer's disease (AD) and is closely associated with amyloid-β (Aβ) pathology. Although compelling experimental data suggest that microglial activation modulates reactive astrogliosis, it remains to be elucidated whether microglial activation influences the association of Aβ pathology with reactive astrogliosis in the living AD human brain. Here, we tested the association of microglial activation and Aβ pathology with reactive astrogliosis in individuals across the aging and AD clinical spectrum.
View Article and Find Full Text PDFBackground: We showed that plasma GFAP (a proxy of astrocyte reactivity) abnormality is key to unleashing Aβ effects on tau phosphorylation in preclinical AD. This suggests that selecting cognitively unimpaired(CU) individuals with both high Aβ and plasma GFAP could offer an early time window in the disease, but with an increased risk of developing tau pathology. Here, we tested the utility of plasma GFAP for population enrichment in clinical trials focusing on CU individuals.
View Article and Find Full Text PDFBiomarkers.
Alzheimers Dement
December 2024
McGill University Research Centre for Studies in Aging, Douglas Research Centre, Montreal, QC, Canada.
Background: Aβ plaques are the first detectable signs of AD pathology. Our group recently demonstrated that the astrocyte activation marker, glial fibrillary acidic protein (GFAP), has a pivotal role in the association between Aβ burden and tau phosphorylation. However, the role of astrocyte activation in individuals that do not present detectable Aβ pathology using biomarkers is still underexplored.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!