Changes to Neurons Hamper the Aging Brain

The good news is that most people in the developed world are living longer; the not-so-good news is that the brain often does not stay sharp in our older age.
Currently, experts do not fully understood why the brain’s cognitive functions such as memory and speech decline as we age. This despite the realization that cognitive decline can be detected before an individual reaches age 50.
Neuroscientists Andy Randall, Ph.D. and Jon Brown, Ph.D. from the University of Bristol have identified a novel cellular mechanism that causes changes to the activity of neurons — an action which may contribute to cognitive decline during normal healthy aging.
The brain largely uses electrical signals to encode and convey information. Modifications to this electrical activity are likely to cause age-dependent changes to cognitive abilities.
The researchers examined the brain’s electrical activity by making recordings of electrical signals in single cells of the hippocampus, a structure with a crucial role in cognitive function. By doing this, they were able to assess “neuronal excitability” – the ease with which a neuron can produce brief, but very large, electrical signals called action potentials.
An action potential occurs in practically all nerve cells and is essential for transmission of a signal or communication within all the circuits of the nervous system.
Action potentials are triggered near the neuron’s cell body and once produced, travel rapidly through the massively branching structure of the nerve cell, along the way activating the synapses the nerve cell makes with the numerous other nerve cells to which it is connected.
Researchers discovered the hippocampal neurons within an aged brain have trouble generating action potentials.
Furthermore, they demonstrated that this relative reluctance to produce action potential arises from changes to the activation properties of membrane proteins called sodium channels. The sodium channels influence the rapid initiation of the action potential by allowing a flow of sodium ions into neurons.
Randall, a professor in applied neurophysiology, said: “Much of our work is about understanding dysfunctional electrical signaling in the diseased brain, in particular Alzheimer’s disease.
“We began to question, however, why even the healthy brain can slow down once you reach my age. Previous investigations elsewhere have described age-related changes in processes that are triggered by action potentials, but our findings are significant because they show that generating the action potential in the first place is harder work in aged brain cells.
“Also by identifying sodium channels as the likely culprit for this reluctance to produce action potentials, our work even points to ways in which we might be able modify age-related changes to neuronal excitability, and by inference cognitive ability.”