Sentence examples for neuronal aging from inspiring English sources

Neuronal aging is unique because neurons are postmitotic cells, and therefore they rely heavily on protein clearance mechanisms to maintain homeostasis.

Some reports suggest that the ability of touch neurons to function correctly is correlated with healthy neuronal aging.

The data support the hypothesis that accumulation of DNA damage and genotoxic stress significantly influences neuronal aging processes and may contribute to motor neuron vulnerability in human neuromuscular disorders.

Despite this potential complexity, Tank and colleagues found that neuronal re-expression of DAF-16 in daf-16 daf-2 daf-16 daf-2ts was sufficient to rescue the doubled onset of neuronal defects observed in daf-2 single mutants, identifying neurons as the cellular focus of DAF-16-mediated control of neuronal aging.

This was observed in both touch receptor and GABAergic neurons, indicating PTL-1 is likely to be a general regulator of neuronal aging.

Recent reports have described progressive morphological changes in C. elegans neurons, - and these phenotypes can be used as parameters to track neuronal aging in the worm.

We found that mature perisynaptic processes are present on both afferent synapses (dendritic spines in the dentate gyrus) and efferent synapses (MFT in the CA3 area) of newly formed neurons, regardless of neuronal age or synapse morphology.

Thus, astrocytic perisynaptic processes ensheathe spine synapses of adult-born neurons and the frequency and distribution of these processes are similar to those of GFP-negative, control neurons and independent of spine morphology or neuronal age.

Interestingly, although the apoptotic pathway becomes blocked with increasing neuronal age, neuronal viability is still affected upon severe hypoxia-ischemia, with many neurons exhibiting features of necrosis rather than classical apoptosis.

Since mean neuronal nuclear diameters were similar across most groups, we can assume that neuronal age was also similar and, hence, that the [H]-thymidine+ neurons were born within the 5 days of treatment.

Together these data suggest that GDNF family members may play a protective role in the gut throughout life, and support the suggestion that dysregulation of neurotrophic factor support could contribute to neuronal ageing in the gut.