Publications by authors named "S C Steininger"
Introduction: Hippocampal atrophy is an established Alzheimer's Disease (AD) biomarker. Volume loss in specific subregions as measurable with ultra-high field magnetic resonance imaging (MRI) may reflect earliest pathological alterations.
Methods: Data from positron emission tomography (PET) for estimation of cortical amyloid β (Aβ) and high-resolution 7 Tesla T1 MRI for assessment of hippocampal subfield volumes were analyzed in 61 non-demented elderly individuals who were divided into risk-categories as defined by high levels of cortical Aβ and low performance in standardized episodic memory tasks.
Background: Effects of beta-amyloid accumulation on neuronal function precede the clinical manifestation of Alzheimer's disease (AD) by years and affect distinct cognitive brain networks. As previous studies suggest a link between beta-amyloid and dysregulation of excitatory and inhibitory neurotransmitters, we aimed to investigate the impact of GABA and glutamate on beta-amyloid related functional connectivity.
Methods: 29 cognitively unimpaired old-aged adults (age = 70.
Alzheimer's disease (AD) is the most common cause of cognitive dysfunction in older adults. The pathological hallmarks of AD such as beta amyloid (Aβ) aggregation and neurometabolic change, as indicated by altered myo-inositol (mI) and N-acetylaspartate (NAA) levels, typically precede the onset of cognitive dysfunction by years. Furthermore, cerebrovascular disease occurs early in AD, but the interplay between vascular and neurometabolic brain change is largely unknown.
View Article and Find Full Text PDFBackground: The incidence of Alzheimer's disease (AD) strongly relates to advanced age and progressive deposition of cerebral amyloid-beta (Aβ), hyperphosphorylated tau, and iron. The purpose of this study was to investigate the relationship between cerebral dynamic functional connectivity and variability of long-term cognitive performance in healthy, elderly subjects, allowing for local pathology and genetic risk.
Methods: Thirty seven participants (mean (SD) age 74 (6.
Article Synopsis
- The study utilized 7 Tesla MRI and PET scans to explore how brain iron levels relate to Amyloid beta (Aβ) plaque accumulation, focusing on individuals at heightened risk for Alzheimer’s disease (AD) due to the APOE-e4 allele and mild cognitive impairment (MCI).
- Carriers of the APOE-e4 allele showed greater Aβ plaque levels in their brains, regardless of their cognitive status, and this association was even more significant in individuals with MCI.
- Additionally, increased levels of brain iron were linked to both higher Aβ plaque loads and functional brain connectivity issues, suggesting that the buildup of iron in the brain might contribute to the progression of neurocognitive dysfunction in Alzheimer’s disease.