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Biomarkers.
Alzheimers Dement
December 2024
Department of Biological Psychology, Vrije Universiteit Amsterdam, Amsterdam, Netherlands.
Background: Plasma biomarkers may be a non-invasive and cost-effective tool for diagnosing Alzheimer's Disease. Promising markers include amyloid-β-42/40 ratio (Aβ-42/40), glial fibrillary acidic protein (GFAP), and neurofilament-light (NfL). Not much is known about what genetic and environmental factors influence and potentially confound these biomarker levels.
View Article and Find Full Text PDFWhite matter hyperintensities (WMH) are areas of increased lucency visualized on T2-weighted magnetic resonance imaging (MRI), including fluid attenuated inversion recovery (FLAIR) sequences. Over the past 15 years we have been examining WMH in studies of cognitive aging among clinical, community-based, and populations at genetic risk to understand the role of vascular brain injury in Alzheimer's disease (AD) onset, symptom progression, and pathogenesis. Our findings suggest that regional WMH, particularly when distributed in posterior areas, increase risk for clinical AD and contribute to the clinical course of the disease, even among genetic population with relatively low rates of vascular risk factor, like adults with Down syndrome and with autosomal dominant genetic mutations for AD.
View Article and Find Full Text PDFBiomarkers.
Alzheimers Dement
December 2024
University of São Paulo Medical School, São Paulo, São Paulo, Brazil.
Background: Down syndrome (DS) is associated with mitochondrial dysfunction leading to higher levels of oxidative stress and cell degeneration. This fact, together with the overexpression of AD-related genes in trisomy 21, increases the risk of developing Alzheimer's disease (AD). Thus, it is important to look for interventions that could prevent mitochondrial damage before symptoms occur.
View Article and Find Full Text PDFBiomarkers.
Alzheimers Dement
December 2024
Brigham and Women's Hospital and Department of Neurology, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA.
Background: Virtually all adults with Down Syndrome(DS) show Alzheimer's disease(AD)-related pathologic change by the age of 40 years. While sex differences in Aβ-dependent tauopathy are apparent during early sporadic AD, sex differences in the DS population remain under-investigated. Moreover, menopause onset occurs earlier in the DS population (45 years), and it remains unknown whether menopause status and hormone therapy(HT) exposure influences Aβ-dependent tauopathy in women with DS.
View Article and Find Full Text PDFBackground: By age 40 years, adults with Down syndrome (DS) develop Alzheimer's disease (AD) pathology and progress to dementia in their 60s. Despite minimal systemic vascular risk factors, individuals with DS have MRI evidence of cerebrovascular injury that progresses with AD severity, suggesting an intrinsic vascular component to DS-AD that may interact with neuroinflammatory processes to promote tau pathology and cognitive decline. In the current study we examined whether cerebrovascular disease (CVD) burden and inflammation/astrocytosis independently and interactively were associated with incident diagnosis among adults with DS.
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