A Brain Changer: How Stress Shapes Cognition and Memory

Some of us have visceral responses to stress—we struggle to focus; our recall is… not great; we feel disorganised, overwhelmed, and exhausted; we can’t sleep; our head hurts, our neck aches; we’re tearful; and we may even feel like we’re on the brink of a meltdown. What does this stress do to the brain, or beneath the skin? Here, we explore the neural mechanisms that underlie how stress and strain shape the brain and its impact on our memory.

The Good, the Bad, and the Ugly

Stress triggers an evolutionary-based, psychobiological response to the precarious environment we find ourselves in on a day-to-day basis. But that is not to say that we cannot experience eustress (more commonly known as “good stress”).

Good stress can elicit excitement—it can be motivating, even performance-enhancing. It can propel us to greater heights during exams, interviews, and speeches. Our pulse hastens, our heart races, our hormones surge—in other words, we feel alive.

Alas, eustress tends to be short-lived. Without it, we can feel listless, rudderless, or just plain unhappy. Good stress is, thus, key to vitality.

But bad stress often creeps up on you like a stranger in the night. It can be chronic in nature or acute and intense. While the healthy brain processes good stress adaptively, bad stress can lead to maladaptive processing with lasting effects on brain structure, function, and plasticity, with changes seen also to neuron shape, connectivity, and cell count. Together, these changes impede cognitive processing (Bremner, 1999).

More Than a Side Effect

Whether on a social or occupational basis, stress can overwhelm cognitive load and evoke aversive neural reactions that disrupt our physiological equilibrium—with knock-on effects seen to our mental well-being and overall health. Stress increases our vulnerability to a range of well-known (and more obscure) physical and mental health conditions—including systemic lupus erythematosus (Morand, 2018), Cushing’s disease (Orsini et al., 2021), cardiovascular disease (Kivimäki & Steptoe, 2018), depression (Hamilton et al., 2021), and psychosis (Dykxhoorn et al., 2020), to name a few.

But what of memory? Deficits in declarative and non-declarative memory (i.e., recall of events and facts vs. conditioning and skill learning), in addition to cognitive difficulty and issues with overall executive function (e.g., flexible thinking and self-control) often coincide with conditions such as these. While they are typically passed off as inconvenient side-effects, there is much more to it than that.

Where Memories Are Made

The hippocampus, amygdala, and prefrontal cortex are crucial components of brain circuitry involved in learning and memory. The hippocampus, however, is the anatomic basis for memory, responsible for memory encoding, consolidation, and retrieval (Lindau et al., 2016).

Although it does not operate in isolation, the hippocampus is the temporal lobe brain structure most sensitive to stress (Calcia et al., 2016). Hippocampal vulnerability stems from the incitement of glucocorticoids and neurotransmitters that are elevated in the stress response (McEwen, 2007). Even in fit and healthy people, stress can elevate glucocorticoids. Soldiers tested at wartime, for example, had excessive levels of urinary cortisol, but notable reductions in cortisol were detected when they were no longer in immediate threat (Howard et al., 1955).

Stress Shrinks the Brain

Stress-induced hippocampal atrophy (aka shrinkage) has been associated with spatial and working memory deficits in both humans and animals (Conrad, 2008). This type of shrinkage occurs through inhibitory effects of prolonged stress exposure on the hypothalamus-pituitary-adrenal (HPA) axis, which causes glucocorticoid hypersecretion and the modulation of excitatory neurotransmitters (McEwenn, 2007).

Chronically elevated glucocorticoids and excitatory amino acid neurotransmitters can permanently alter brain architecture. This level of exposure can cause a number of neuronal changes, from reduced dendritic branching, synaptic terminal structural alterations, neuron death, and neuronal regeneration inhibition in the hippocampus (Bremner, 1999).