Abstract
Aging is associated with a general decline in cognitive functions, which appears to be due to alterations in the amounts of proteins involved in the regulation of synaptic plasticity. Here, we present a quantitative analysis of proteins involved in neurotransmission in three brain regions, namely, the hippocampus, the cerebral cortex and the cerebellum, in mice aged 1 and 22 months, using the total protein approach technique. We demonstrate that although the titer of some proteins involved in neurotransmission and synaptic plasticity is affected by aging in a similar manner in all the studied brain formations, in fact, each of the formations represents its own mode of aging. Generally, the hippocampal and cortical proteomes are much more unstable during the lifetime than the cerebellar proteome. The data presented here provide a general picture of the effect of physiological aging on synaptic plasticity and might suggest potential drug targets for anti-aging therapies.
Highlights
Physiological aging is related to a gradual decline in cognitive functions, such as memory formation and retention, processing speed and conceptual reasoning [1]
Our analysis demonstrated that the total concentration of the GABAA protein was significantly reduced in the hippocampus and cortex of old mice, but it was not affected by aging in the cerebellum (Figure 2A)
We found that among Camk2 isoforms, the titer of Camk2a is the highest in all the studied brain structures (Figure 3A–D), and that its concentration in the hippocampus and cortex is many times higher than the titer of Camk2b, the second most abundant isoform of Camk2 (Figure 3A,B)
Summary
Physiological aging is related to a gradual decline in cognitive functions, such as memory formation and retention, processing speed and conceptual reasoning [1]. It has been demonstrated that aging is associated with the shortening of dendrites and a decrease in their number, loss of dendritic spines, a decrease in the axon number within a network and the level of their myelination and loss of synapses [5]. It has been shown that the molecular mechanisms underlying brain plasticity phenomena such as long-term potentiation and depression of the glutamatergic (LTP and LTD) and GABAergic (iLTP and iLTD) synapses and the efficacy of various neuromodulator systems decline with advancing age [6,7]. Several studies have demonstrated that aging-related cognitive changes are accompanied by changes in the expression and/or localization of proteins involved in synaptic transmission and plasticity [6,8]. The expression of proteins in various regions of the rodent brain has been intensively studied by mass spectrometry-based proteomic techniques [9,10]
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