Stressed brains age faster

Memory formed by dendritic spines
Many dendrites extending out from a neuron body (in the upper right hand corner ). Image by By Patrick Pla via Wikimedia commons

It’s an unfortunate fact of life that as we age our brain stops working as well as we would like. It’s harder to learn new things and remember the things we used to know. This is made worse by chronic stress.

Cortisol is a hormone released by the adrenal gland in response to stress. It’s the ‘fight or flight’ hormone. It gets the body madly making glucose to use as energy to fight or flee whatever is stressing us. It also activates anti-inflammatory and anti-stress mechanisms inside our cells.

Long term stress causes cortisol levels to be chronically increased. Increased cortisol levels can cause problems with short term working memory. It makes it harder to remember and process information. This is because cortisol exposure decreases the number and shape of dendritic spines in the frontal cortex of the brain – where short term memories are housed and processed.

Dendrites are the ‘arms’ branching off from neurons that carry messages to other neurons. Each dendrite can form many little spines called dendritic spines. These spines form connections with other neurons called synapses. Synapses allow messages to be transferred from one neuron to another. This is the basis of how our brain works. Less dendritic spines means less connections between neurons. Lowering stress can completely reverse these changes in young animals, but not in aged animals. In fact aged animals, whether stressed or not, have less dendritic spines than young animals.

So the question is whether cortisol, the stress hormone, is causing the age-related deterioration in dendritic spines? To answer this question, scientists looked at the naturally occurring cortisol levels in young (four month) and old (21 month) rats. They found that some animals had higher than average cortisol levels and some animals had lower hormone levels. The animals with higher cortisol had bigger adrenal glands and less dendritic spines.

Overall the aged rats had 11% less dendritic spines than young rats. Stress made this ageing effect much worse. Old stressed animals, with high cortisol levels, had 20% less dendritic spines than young animals, but also 20% less than old animals with low cortisol. Put another way, the old unstressed animals had the same number of dendritic spines as young animals. Cortisol did not affect dendritic spine number in young animals – they were resistant to this effect of the stress hormone. This means that the loss in dendritic spines may have been caused by a chronic increase in cortisol levels. Or it may be that aged animals have lost the ability to compensate for increased cortisol.

Most of the spine loss in the old stressed animals was a loss of thin spines. Thin dendritic spines are newly made neuronal connections. This lack of thin spines showed that the old stressed brains were less able to make new connections, so were less able to learn and remember. The old stressed animals also had shorter dendritic spines i.e. weaker communication between neurons.

The scientists then tested whether these structural brain changes translated into real deficits in memory and thinking. They trained the rats how to use a maze. All old animals were slower to make decisions about which way to go in the maze and made less right decisions than young animals. This was markedly worse in the old stressed animals than the old unstressed animals.

All of the rats in this study were housed in the same conditions. So I think the biggest question this paper raises is why are some animals in the same environment more stressed than others? And more importantly how can we decrease that stress?

The Scientific Paper:
Anderson et al. Adrenocortical status predicts the degree of age-related deficits in prefrontal structural plasticity and working memory. J. Neurosci. 2014

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