The phrase "aging neuron" is correct and usable in written English.
It can be used in discussions related to neuroscience, biology, or aging, particularly when referring to the changes that occur in neurons as they age.
Example: "Research has shown that aging neurons exhibit reduced synaptic plasticity, which can impact cognitive function."
Alternatives: "maturing neuron" or "senescent neuron".
Progressive DNA damage and decreased PARP-1 activity in aging neurons eventually leads to programmed neuronal death and loss of memory consolidation.
Genetic defects in genes encoding docking proteins have the potential to cause abnormal interaction with the RET signaling, which in turn may result in aging neurons and contribute to aging-related disorders such as Parkinson's disease [ 34] and Alzheimer's disease [ 35].
Persistent increases in cytosolic intracellular Ca2+ concentrations in aging neurons are associated with learning impairments, while small transient subcellular changes in intracellular calcium concentrations play critical roles in neural plasticity in young neurons.
An altered [Ca2+]i homeostasis in aging neurons can have important functional consequences and impair synaptic plasticity as well as learning or memory [102].
During aging, neurons are subject to increased oxidative stress and impaired energy metabolism, leading to dysfunction of proteins responsible for maintaining proper membrane excitability and subcellular Ca2+ dynamics [28].
We report that in aging neurons and 3xTg-AD neurons, NAD(P H depletion is more seminal for neurodegeneration than GSH.
Future work carefully examining the metabolic profiles of diseased and aging neurons may help delineate pathogenic mechanisms and potential therapeutic approaches.
More explicit, a recent study hypothesizes that in aging neurons down-regulation of FKBP12 activates mTOR and enhances RyR mediated Ca2+ release [ 5], explaining the Ca2+ signal phenotype typical of aged neurons [ 12].
An increase in oxidized protein levels in our model and evidence for dysfunction in the ubiquitin-proteasome system in aging and neurodegenerative disease supports a significant role for protein homeostasis mechanisms in maintaining functional integrity in aging neurons.
In other examples, the S. cerevisiae LTR RTE Ty1 is mobilized during chronological aging of this species [ 41], and several D. melanogaster LINE and LTR RTEs become active in aging neurons [ 42].
