Glial cells express a bewildering array of neurotransmitter receptors. To illustrate the complexity of expression, we have assayed non-glutamatergic neurotransmitter receptor mRNA in isolated rat optic nerve, a preparation devoid of neurons and neuronal synapses and from which relatively pure "glial" RNA can be isolated. Of the 44 receptor subunits examined which span the GABA-A, nicotinic, adreno- and glycine receptor families, over three quarters were robustly expressed in this mixed population of white matter glial cells, with several expressed at higher levels than found in control whole brain RNA. In addition to the complexity of glial receptor expression, numerous neurotransmitter release mechanisms have been identified. We have focused on glutamate release from astrocytes, which can occur via at least seven distinct pathways and which is implicated in excitotoxic injury and are neurons and glia. Recent findings suggest that non-glutamatergic receptors can also mediate acute glial injury are also discussed.
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http://dx.doi.org/10.1016/j.neuint.2010.03.024 | DOI Listing |
Alzheimers Dement
December 2024
The TT & WF Chao Center for BRAIN and Houston Methodist Neal Cancer Center, Houston Methodist Hospital, Houston, TX, USA.
Background: Global epidemiological studies involving over nine million participants have shown a 35% lower incidence of Alzheimer's Disease (AD) in older cancer survivors compared to those without a history of cancer. This inverse relationship, consistent across recent studies with methodological controls, suggests that cancer itself, rather than cancer treatments, may offer protective factors against AD. This insight opens avenues for novel therapeutic strategies targeting early AD by harnessing cancer-associated protective factors.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Division of Neurodegenerative Disorders, St. Boniface Hospital Albrechtsen Research Centre, Winnipeg, MB, Canada.
Background: Alzheimer's disease (AD) is a neurodegenerative disorder primarily associated with aging, but manifests as a complex interplay of multiple factors. Decline in sex-hormones, particularly 17-beta estradiol, is linked to the aging process. The risk for onset of AD significantly increases with aging and loss of estradiol.
View Article and Find Full Text PDFBackground: Evidence suggests glucagon-like peptide 1 receptor agonists (GLP-1RAs) may have therapeutic potential in Alzheimer's disease (AD). Cumulative evidence has indicated a potential reduction in cognitive decline in people with AD, while real-world evidence has shown decreased dementia risk in patients with type 2 diabetes. Non-clinical data reveal that GLP-1RAs impact neuroinflammation and other biological processes believed to be involved in AD pathophysiology, including effects on central and peripheral immune cells.
View Article and Find Full Text PDFBackground: A 73-year-old female with a 3 year history of Alzheimer's disease was treated within the protocol of The Alzheimer's Autism and Cognitive Impairment Stem Cell Treatment Study (ACIST), an IRB approved clinical study registered with clinicaltrials.gov NCT03724136.
Method: The procedure consists of bone marrow aspiration, cell separation using an FDA cleared class 2 device, and intravenous and intranasal administration of the stem cell fraction.
This study characterizes a fluorescent -tdTomato neuronal reporter mouse line with strong labeling of axons throughout the optic nerve, of retinal ganglion cell (RGC) soma in the ganglion cell layer (GCL), and of RGC dendrites in the inner plexiform layer (IPL). The model facilitated assessment of RGC loss in models of degeneration and of RGC detection in mixed neural/glial cultures. The tdTomato signal showed strong overlap with >98% cells immunolabeled with RGC markers RBPMS or BRN3A, consistent with the ubiquitous presence of the vesicular glutamate transporter 2 (VGUT2, SLC17A6) in all RGC subtypes.
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