Age-dependence and aging-dependence: The case of neuronal loss and lifespan in a<i>C. elegans</i>model of Parkinson’s disease

It is often assumed, but not established, that the major neurodegenerative diseases, such as Parkinson’s disease, are not just age-dependent (their incidence changes with time) but actually aging-dependent (their incidence is coupled to the process that determines lifespan). To determine a dependence on the aging process requires the joint probability distribution of disease onset and lifespan. For human Parkinson’s disease, such a joint distribution is not available because the disease cuts lifespan short. To acquire a joint distribution, we resorted to an establishedC. elegansmodel of Parkinson’s disease in which the loss of dopaminergic neurons is not fatal. We find that lifespan is not correlated with the loss of neurons and that a lifespan-extending intervention into insulin/IGF1 signaling accelerates neuronal loss, while leaving death and neuronal loss times uncorrelated. This suggests that distinct and compartmentalized instances of the same genetically encoded insulin/IGF1 signaling machinery act independently to control neurodegeneration and lifespan inC. elegans. Although the human context might well be different, our study calls attention to maintaining a rigorous distinction between age-dependence and aging-dependence..

Medienart:	Preprint

Erscheinungsjahr:	2022
Erschienen:	2022

Enthalten in:	bioRxiv.org - (2022) vom: 20. Juli Zur Gesamtaufnahme - year:2022

Sprache:	Englisch

Beteiligte Personen:	Apfeld, Javier [VerfasserIn] Fontana, Walter [VerfasserIn]

Links:	Volltext [lizenzpflichtig] Volltext [kostenfrei]

doi:	10.1101/098038

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PPN (Katalog-ID):	XBI000102113