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Basic Science and Pathogenesis.
Alzheimers Dement
December 2024
VIB-UGent Center for Inflammation Research, Ghent, Belgium.
Background: The brain is shielded from the peripheral circulation by central nervous system (CNS) barriers, comprising the well-known blood-brain barrier (BBB) and the less recognized blood-cerebrospinal fluid (CSF) barrier located within the brain ventricles. The gut microbiota represents a diverse and dynamic population of microorganisms that can influence the health of the host, including the development of neurological disorders like Alzheimer's disease (AD). However, the intricate mechanisms governing the interplay between the gut and brain remain elusive, and the means by which gut-derived signals traverse the CNS barriers remain unclear.
View Article and Find Full Text PDFBasic Science and Pathogenesis.
Alzheimers Dement
December 2024
Department of Pediatrics, Division of Infectious Diseases and Immunology, Cedars-Sinai Medical Center, Los Angeles, CA, USA.
Background: Alzheimer's disease (AD) is a progressive irreversible dementia characterized by beta-amyloid protein plaque deposition and hyperphosphorylation of tau forming neurofibrillary tangles, and neurodegeneration. An emerging theory posits that infections could be one of the triggering factors in AD development and progression. Multiple lines of evidence have linked Chlamydia pneumoniae (Cp), a gram-negative obligate intracellular bacterium with AD.
View Article and Find Full Text PDFBasic Science and Pathogenesis.
Alzheimers Dement
December 2024
Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA.
Background: One of the major outstanding questions in the field of Alzheimer's disease (AD) research is the underlying mechanism by which APOE ε4, the strongest genetic risk factor for AD, contributes to disease pathogenesis. Current therapies targeting amyloid-beta plaques show modest effect in non-APOE4 male AD patients, and greatly increase the risk for amyloid-related imaging abnormalities - edema/effusion (ARIA-E) in APOE ε4 carriers. We made an important discovery that APOE4 neutrophil-microglia interactions drive cognitive impairment in a sex-dependent manner.
View Article and Find Full Text PDFBasic Science and Pathogenesis.
Alzheimers Dement
December 2024
University of British Columbia, Vancouver, BC, Canada.
Background: Our current understanding of the molecular mechanisms underlying amyloidogenesis in Alzheimer's Disease (AD) is limited by the lack of comprehensive models closely resembling human pathology. Human induced pluripotent stem cell (hiPSC) 3-dimensional (3D) models, such as brain organoids and neurospheres, are emerging as innovative approaches to model neurodegenerative diseases in vitro. However, they rely on hiPSC self-organization and are therefore characterized by low reproducibility and homogeneity.
View Article and Find Full Text PDFBasic Science and Pathogenesis.
Alzheimers Dement
December 2024
University of British Columbia, Vancouver, BC, Canada.
Background: Murine models of Alzheimer's Disease (AD) have resulted in numerous discoveries leading to a better understanding of AD pathogenesis but results poorly translated to novel treatment options. Over the past years, iPSC-derived human neuronal cultures have been developed to better model AD in vitro. One key hallmark of AD is the presence of insoluble Aß plaques in the brain.
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