Good news! Towards the fountain of youth!
"A protein involved in Alzheimer’s-disease progression has been linked to normal brain ageing, suggesting that researchers could target it to stave off age-related mental decline. The breakdown of amyloid-β precursor protein (APP), creates amyloid-β peptides, which are often present in plaques in the brains of people with Alzheimer’s disease. Researchers found that knocking out the gene that produces APP in turquoise killifish (Nothobranchius furzeri) reduces signs of ageing — hinting that it has an overlooked role in neurodegeneration that isn’t caused by disease."
From the abstract:
"Brain aging is a pivotal risk factor for many neurodegenerative diseases, yet its molecular and cellular mechanisms remain elusive. The amyloid-beta precursor protein (APP) is among the most studied proteins linked to brain pathology; however, its role in non-pathological brain aging remains poorly characterized. Here, we investigate the natural impact of APP on normal brain aging using the short-lived turquoise killifish (Nothobranchius furzeri), which exhibits rapid and spontaneous age-related decline. We found that pyroglutamated amyloid beta —a neurotoxic Aβ variant—accumulates intra-neuronally in an age-dependent manner, co-localizing with a marker of cell death.
We found that intraneuronal pyroglutamated amyloid beta is also present in old human brains, suggesting deep evolutionary conservation.
To determine Aβ’s role in spontaneous brain aging, we generated an “amyloid precursor protein a” (appa) knock-out killifish line using CRISPR/Cas9. The knock-out of appa rescued age-dependent increase in cell death and inflammation, mitigated proteome-wide brain aging and improved the age-related decline in neuronal activity and learning capacity. Our findings show a key role for Aβ precursor protein in non-pathological brain aging, making it a suitable target for anti-aging interventions."
This key protein could be responsible for brain ageing "An amyloid protein targeted by Alzheimer’s disease therapies seems to be involved in normal mental decline."
APP contributes to brain aging and learning decline in short-lived turquoise killifish (original news release, but extremely short) "Brain aging is influenced by the amyloid-beta precursor protein (APP), which accumulates in the brain and contributes to cell death and inflammation. ... found that knocking out APP in a short-lived fish species improved brain health and reduced age-related decline, suggesting a potential target for anti-aging interventions."
3D protein structure of amyloid beta (1-42) is conserved between turquoise killifish and humans.
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