AI Article Synopsis
- Alzheimer's disease leads to early loss of cholinergic neurons and reduced nerve growth factor (NGF), making NGF delivery via encapsulated cell bio-delivery (ECB) a potential treatment option.
- Previous studies showed variability in long-term viability and NGF release from ECB, prompting investigations into the effects of amyloid beta-peptides, interleukin 1-beta, and cerebrospinal fluid from various dementia patients on NGF-producing cell lines.
- Results indicated that while amyloid beta had no significant effect, interleukin 1-beta reduced NGF production, and cerebrospinal fluid from Alzheimer's patients significantly decreased NGF release compared to other conditions, highlighting inflammation's negative impact on ECB cell
Article Abstract
Alzheimer's disease (AD) is characterized by early degeneration of cholinergic neurons and decreased levels of nerve growth factor (NGF). Thus, increasing the NGF levels by for instance encapsulated cell bio-delivery (ECB) is a potential treatment strategy. The results from our previous first-in-human studies on ECB of NGF to the basal forebrain cholinergic neurons were promising, but indicated some variability of long-term viability of the encapsulated cells and associated reduced NGF-release. Here we studied the effect of amyloid beta-peptides (Aβ), interleukin 1-beta (IL-1β), and CSF from AD, Lewy body dementia (LBD) or subjective cognitive impairment (SCI) patients on the NGF overproducing cell line NGC-0295. At physiological concentrations, neither Aβ nor Aβ had any major impact on cell viability or NGF-production. In contrast, IL-1β dose-dependently affected NGF-production over time. Exposure of NGF-producing cells to CSF from AD patients showed significantly reduced NGF-release as compared to CSF from LBD or SCI patients. By mass spectrometry we found 3 proteins involved in inflammatory pathways to have an altered expression in AD CSF compared to LBD and SCI. Cell survival and NGF-release were not affected by Aβ. NGF-release was affected by IL-1β, suggesting that inflammation has a negative effect on ECB cells.
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| http://dx.doi.org/10.1016/j.yexcr.2018.08.007 | DOI Listing |
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