Physio-pathological conditions such as neuroinflammation can modulate neurogenesis in the hippocampus. The aim of this study is to follow the time course of inflammation-induced effects on the neurogenic niche and the counter-effects of an anti-inflammatory drug. Rats received intracerebroventricular injections of lipopolysaccharide/endotoxin (ET) and intraperitoneal injections of 5'-bromo-2'-deoxyuridine, then perfused at different time intervals. At day 3, ET injection resulted in thermal hyperalgesia accompanied by a significant decrease in neurogenesis. A rebound of neurogenesis was detected at day 6 and levels were back to basal at day 9. Daily treatment with Piroxicam alleviated the ET-induced effects.
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http://dx.doi.org/10.1016/j.jneuroim.2017.12.013 | DOI Listing |
Alzheimers Dement
December 2024
Neurophysiology & Behaviour Lab, University of Castilla‐La Mancha, Ciudad Real, Spain
Background: A key neuropathological feature in the early stages of Alzheimer's disease (AD) involves hippocampal dysfunction arising from the accumulation of amyloid‐β (Aβ). Previously, our laboratory identified a shift in the synaptic plasticity long term potentiation (LTP)/long term depression (LTD) induction threshold, leading to memory deficits in a non‐transgenic murine model of early AD generated by intracerebroventricular (icv.) injections Aβ oligomers (oAβ), one of the most predominant pathogenetic factors in initial stages of the disease.
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December 2024
Brain and Spine Surgeons of Orange County, Newport Beach, CA, USA
Background: It has been more than 20 years for a new treatment for Alzheimer’s Disease (AD) to emerge. This treatment has recently been in the form of a monoclonal antibody targeting the end‐products of neuronal death. We are testing the safety of a novel approach using activated stem cells injected directly into the ventricles of the brain.
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December 2024
Feinstein Institutes for Medical Research, Manhasset, NY, USA
Background: While A1 astrocytes are reported in Alzheimer’s disease (AD), the underlying molecular mechanisms are complex and remain elusive. Proinflammatory extracellular cold‐inducible RNA‐binding protein (eCIRP) is released by microglia in response to AD‐associated neuronal amyloid‐β. eCIRP activates the triggering receptor expressed on myeloid cells‐1 (TREM‐1).
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December 2024
Shoolini University, Solan, Himachal Pradesh, India
Background: Alzheimer’s disease (AD) is a complex neurodegenerative disorder characterized by progressive cognitive decline, neuroinflammation, and mitochondrial dysfunction. In Alzheimer’s, abnormal Mitochondrial Permeability Transition Pore (mPTP) activity may contribute to mitochondrial dysfunction and neuronal damage. Withanolide A, a naturally occurring compound derived from , have shown potential neuroprotective effects in various neurological disorders.
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December 2024
Federal University of Minas Gerais, Belo Horizonte, Minas Gerais, Brazil
Background: Acetylcholine, a neurotransmitter critical for cognitive functions, including attention, memory, and sociability, is essential for maintaining synaptic integrity. Deficits in acetylcholine levels are linked to cognitive impairments. Heterozygous VAChT KD (VAChT KDHET) mice, characterized by reduced vesicular acetylcholine transporter protein production, exhibit cognitive impairments due to diminished acetylcholine release.
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