This protocol describes the differentiation of human neural progenitor cells (hNPCs) in a microfluidic device containing a thin 3D matrix with two separate chambers, enabling a cleaner separation between axons and soma/bulk neurons. We have used this technique to study how mitochondria-associated ER membranes (MAMs) regulate the generation of somal and axonal amyloid β (Aβ) in FAD hNPCs, a cellular model of Alzheimer's disease. This protocol also details the quantification of Aβ molecules and isolation of pure axons via axotomy. For complete details on the use and execution of this profile, please refer to Bhattacharyya et al. (2021).
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http://dx.doi.org/10.1016/j.xpro.2021.101028 | DOI Listing |
Neurochem Res
January 2025
Department of Neurology, Affiliated Hospital of Zunyi Medical University, Zunyi, China.
Alzheimer's disease (AD) is a central nervous system degenerative disease with a stealthy onset and a progressive course characterized by memory loss, cognitive dysfunction, and abnormal psychological and behavioral symptoms. However, the pathogenesis of AD remains elusive. An increasing number of studies have shown that oligodendrocyte progenitor cells (OPCs) and oligodendroglial lineage cells (OLGs), especially OPCs and mature oligodendrocytes (OLGs), which are derived from OPCs, play important roles in the pathogenesis of AD.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
STEM Neurology & Neuropsychological0 Research Group Egypt (SNRGE), Port Said, Port Said, Egypt.
Background: The olfactory mucosa cells are capable of lifelong neurogenesis providing a viable source of progenitor cells. Olfactory mucosa progenitor cells (OMPCs) have alleviated several cerebral ischemia/reperfusion damage markers. OMPCs are safely obtainable from the upper nasal cavity.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Icahn School of Medicine at Mount Sinai, New York, NY, USA.
Background: The accumulation of abnormal tau protein in neurons and glia in the human brain is the defining feature of neurodegenerative diseases known as tauopathies. Progressive supranuclear palsy (PSP), the most common primary tauopathy, is typified by selective vulnerability of dopaminergic neurons and glia in the midbrain leading to an atypical parkinsonian movement disorder. To investigate candidate disease mechanisms underlying PSP, there is a critical need for model systems that more accurately recapitulate the cellular and molecular environment in the human brain.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
University of Kansas Medical Center, Kansas City, KS, USA.
Background: Mitochondrial dysfunction is an early and prominent feature of Alzheimer's disease (AD). We have recently published that lower brain mitochondrial DNA copy number (mtDNAcn) is associated with increased risk of AD neuropathological change and reduced cognitive performance. Here, we addressed how mtDNAcn affects cell-type specific phenotypes.
View Article and Find Full Text PDFAlzheimers 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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