In a novel animal study design that mimicked human clinical trials, researchers at University of California, San Diego School of Medicine report that long-term treatment using a small molecule drug that reduces activity of the brain's stress circuitry significantly reduces Alzheimer's disease (AD) neuropathology and prevents onset of cognitive impairment in a mouse model of the neurodegenerative condition.
Previous research has shown a link between the brain's stress signaling pathways and AD. Specifically, the release of a stress-coping hormone called corticotropin-releasing factor (CRF), which is widely found in the brain and acts as a neurotransmitter/neuromodulator, is dysregulated in AD and is associated with impaired cognition and with detrimental changes in tau protein and increased production of amyloid-beta - protein fragments that clump together and trigger the neurodegeneration characteristic of AD.
My turn:
Lipopolysaccharide (LPS) increases plasma levels of CRF in rats.
Chronic LPS administration increases Beta amyloid levels in the brains of mice.
