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Now showing items 11-15 of 15
1-42 beta-Amyloid peptide requires PDK1/nPKC/Rac 1 pathway to induce neuronal death
(Nature Publishing Group, 2013-01)
1-42 beta-Amyloid (A beta(1-42)) peptide is a key molecule involved in the development of Alzheimer's disease. Some of its effects are manifested at the neuronal morphological level. These morphological changes involve ...
Oligodendrocyte differentiation from adult multipotent stem cells is modulated by glutamate
(Nature Publishing Group, 2012-02)
We used multipotent stem cells (MSCs) derived from the young rat subventricular zone (SVZ) to study the effects of glutamate in oligodendrocyte maturation. Glutamate stimulated oligodendrocyte differentiation from SVZ-derived ...
Contribution of Neurons and Glial Cells to Complement-Mediated Synapse Removal during Development, Aging and in Alzheimer’s Disease
(Hindawi, 2018)
Synapse loss is an early manifestation of pathology in Alzheimer's disease (AD) and is currently the best correlate to cognitive decline. Microglial cells are involved in synapse pruning during development via the complement ...
A Neuron, Microglia, and Astrocyte Triple Co-culture Model to Study Alzheimer’s Disease
(Frontiers Media, 2022-04-14)
Glial cells are essential to understand Alzheimer's disease (AD) progression, given their role in neuroinflammation and neurodegeneration. There is a need for reliable and easy to manipulate models that allow studying the ...
A nonlinear meccano for Alzheimer's emergence by amyloid β-mediated glutamatergic hyperactivity
(Elsevier, 2024-05)
The pathophysiological process of Alzheimer's disease (AD) is believed to begin many years before the formal diagnosis of AD dementia. This protracted preclinical phase offers a crucial window for potential therapeutic ...