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http://dx.doi.org/10.1016/j.ijcard.2017.12.079 | DOI Listing |
Cerebellum
January 2025
Department of Neurology, Kailuan General Hospital, No. 57 Xinhua East Road, Lubei District, Tangshan City, 063000, Hebei Province, China.
This study aims to evaluate cognitive impairments in patients with acute cerebellar infarction using event-related potentials (ERP) and electrophysiological source imaging (ESI). Thirty patients with acute cerebellar infarction and 32 healthy volunteers were selected. Cognitive potentials were recorded and measured using a visual Oddball paradigm.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
University of Connecticut, Storrs, CT, USA.
Background: With insight into the elevated levels of phosphorylation of diseased tau, it is believed that specific modifications occur in a time-dependent manner that contribute to tau's role in Alzheimer's disease pathogenesis and progression. Present methods to obtain phospho-tau (p-tau) from post-mortem tissue or recombinantly are insufficient to answer the foremost questions in the field, and there is currently no way to study each disease-relevant modification reproducibly or in isolation. To this point, learning about tau phosphorylation at the resolution of a single modification has been a major obstacle in clarifying whether certain sites are causative of disease or just a by-product of other harmful mechanisms.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Department of Pathology and Laboratory Medicine, University of Pennsylvania Perelman School of Medicine, Philadelphia, PA, USA.
Background: Recent studies suggest genome-wide-association-studies (GWAS) loci confer their effects on microglia in late-onset Alzheimer's disease (LOAD) brains. Relatively fewer studies have investigated the effects of other genome-wide significant loci (p<5e) using human neurons.
Method: GWAS itself cannot directly identify causal variant-(effector)gene-pairs as GWAS only reports the sentinel variant at a given locus.
Alzheimers Dement
December 2024
Ohio State University College of Medicine, Neurobiology of Aging & Resilience Center, Columbus, OH, USA.
Background: The cerebrovasculature is an essential component of brain homeostasis. Cerebrovascular disorders are associated with an increased risk for neurodegenerative diseases, including Alzheimer's disease (AD). However, the mechanisms by which cerebrovascular dysfunction contributes to neurodegeneration are poorly understood.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
University of Pennsylvania, Philadelphia, PA, USA.
Background: To date, Alzheimer's disease (AD) research has principally focused on neurons. In contrast, recent studies suggest that genetic mechanisms drive microglia towards prolonged inflammation in AD brains, exacerbating neurodegeneration. Indeed, many of the 70 disease-associated loci uncovered with genome-wide association studies (GWAS) reside near genes related to microglial function, such as TREM2.
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