Publications by authors named "Armand Gonzalez Escalante"
Article Synopsis
- Recent advancements in Alzheimer's treatment now require verification of amyloid-β pathology using PET scans or cerebrospinal fluid, but blood tests could simplify this process.* -
- A study involving nearly 7,000 individuals identified that the plasma biomarker p-tau217 can reliably indicate amyloid-β pathology, especially in patients with probable Alzheimer’s dementia.* -
- The findings suggest that combining p-tau217 results with clinical assessments may allow for accurate diagnoses without the need for more invasive PET or CSF tests.*
Introduction: We examined whether baseline glial markers soluble triggering receptor expressed on myeloid cell 2 (sTREM2), chitinase 3-like protein 1 (YKL-40), and glial fibrillary acidic protein (GFAP) in cerebrospinal fluid (CSF), and plasma GFAP are associated with cognitive change in cognitively unimpaired (CU) individuals at risk of Alzheimer's disease (AD).
Methods: A total of 353 CU (mean age 60.9 years) participants were included (mean follow-up time 3.
The mediating role of neuroimaging-derived biological brain age in the association between risk factors for dementia and cognitive decline in middle-aged and older individuals without cognitive impairment: a cohort study.
Lancet Healthy Longev
April 2024
Background: Neuroimaging-based brain-age delta has been shown to be a mediator linking cardiovascular risk factors to cognitive function. We aimed to assess the mediating role of brain-age delta in the association between modifiable risk factors of dementia and longitudinal cognitive decline in middle-aged and older individuals who are asymptomatic, stratified by Alzheimer's disease pathology. We also explored whether the mediation effect is specific to cognitive domain.
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- The ALzheimer's and FAmilies (ALFA) project started in 2013 to explore early signs and genetic factors of Alzheimer's disease (AD) to aid in detection and prevention.
- The study involved a detailed genetic analysis of participants, focusing on aspects like amyloid/tau status and included gender differences, and compared findings with data from the Alzheimer's Disease Neuroimaging Initiative (ADNI).
- Results indicate ALFA successfully formed a group of cognitively healthy individuals who are at a heightened genetic risk for AD, making it an ideal setting for studying early changes in the disease's progression.
Introduction: Detection of Alzheimer's disease (AD) pathophysiology among individuals with mild cognitive changes and those experiencing subjective cognitive decline (SCD) remains challenging. Plasma phosphorylated tau 217 (p-tau217) is one of the most promising of the emerging biomarkers for AD. However, accessible methods are limited.
View Article and Find Full Text PDFIntroduction: We studied how biomarkers of reactive astrogliosis mediate the pathogenic cascade in the earliest Alzheimer's disease (AD) stages.
Methods: We performed path analysis on data from 384 cognitively unimpaired individuals from the ALzheimer and FAmilies (ALFA)+ study using structural equation modeling to quantify the relationships between biomarkers of reactive astrogliosis and the AD pathological cascade.
Results: Cerebrospinal fluid (CSF) amyloid beta (Aβ) was associated with Aβ aggregation on positron emission tomography (PET) and with CSF p-tau , which was in turn directly associated with CSF neurofilament light (NfL).
Blood biomarkers indicating elevated amyloid-β (Aβ) pathology in preclinical Alzheimer's disease are needed to facilitate the initial screening process of participants in disease-modifying trials. Previous biofluid data suggest that phosphorylated tau231 (p-tau231) could indicate incipient Aβ pathology, but a comprehensive comparison with other putative blood biomarkers is lacking. In the ALFA+ cohort, all tested plasma biomarkers (p-tau181, p-tau217, p-tau231, GFAP, NfL and Aβ42/40) were significantly changed in preclinical Alzheimer's disease.
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