Reviving a failing sense of smell through training

January, 2012

A rat study reveals how training can improve or impair smell perception.

The olfactory bulb is in the oldest part of our brain. It connects directly to the amygdala (our ‘emotion center’) and our prefrontal cortex, giving smells a more direct pathway to memory than our other senses. But the olfactory bulb is only part of the system processing smells. It projects to several other regions, all of which are together called the primary olfactory cortex, and of which the most prominent member is the piriform cortex. More recently, however, it has been suggested that it would be more useful to regard the olfactory bulb as the primary olfactory cortex (primary in the sense that it is first), while the piriform cortex should be regarded as association cortex — meaning that it integrates sensory information with ‘higher-order’ (cognitive, contextual, and behavioral) information.

Testing this hypothesis, a new rat study has found that, when rats were given training to distinguish various odors, each smell produced a different pattern of electrical activity in the olfactory bulb. However, only those smells that the rat could distinguish from others were reflected in distinct patterns of brain activity in the anterior piriform cortex, while smells that the rat couldn’t differentiate produced identical brain activity patterns there. Interestingly, the smells that the rats could easily distinguish were ones in which one of the ten components in the target odor had been replaced with a new component. The smells they found difficult to distinguish were those in which a component had simply been deleted.

When a new group of rats was given additional training (8 days vs the 2 days given the original group), they eventually learned to discriminate between the odors the first animals couldn’t distinguish, and this was reflected in distinct patterns of brain activity in the anterior piriform cortex. When a third group were taught to ignore the difference between odors the first rats could readily distinguish, they became unable to tell the odors apart, and similar patterns of brain activity were produced in the piriform cortex.

The effects of training were also quite stable — they were still evident after two weeks.

These findings support the idea of the piriform cortex as association cortex. It is here that experience modified neuronal activity. In the olfactory bulb, where all the various odors were reflected in different patterns of activity right from the beginning (meaning that this part of the brain could discriminate between odors that the rat itself couldn’t distinguish), training made no difference to the patterns of activity.

Having said that, it should be noted that this is not entirely consistent with previous research. Several studies have found that odor training produces changes in the representations in the olfactory bulb. The difference may lie in the method of neural recording.

How far does this generalize to the human brain? Human studies have suggested that odors are represented in the posterior piriform cortex rather than the anterior piriform cortex. They have also suggested that the anterior piriform cortex is involved in expectations relating to the smells, rather than representing the smells themselves. Whether these differences reflect species differences, task differences, or methodological differences, remains to be seen.

But whether or not the same exact regions are involved, there are practical implications we can consider. The findings do suggest that one road to olfactory impairment is through neglect — if you learn to ignore differences between smells, you will become increasingly less able to do so. An impaired sense of smell has been found in Alzheimer’s disease, Parkinson's disease, schizophrenia, and even normal aging. While some of that may well reflect impairment earlier in the perception process, some of it may reflect the consequences of neglect. The burning question is, then, would it be possible to restore smell function through odor training?

I’d really like to see this study replicated with old rats.

Reference: 

Related News

A study involving 614 patients with type 2 diabetes (mean age 62) has found that longer duration of diabetes was associated with more brain volume loss, particularly in the gray matter.

Type 2 diabetes greatly increases a person's risk of developing cardiovascular disease, but a new study shows that cardiovascular risk factors such as elevated blood pressure and cholesterol levels differ significantly between men and women with diabetes.

A mouse study has found that introduction of oral bacteria into the bloodstream increased risk factors for atherosclerotic heart disease, including cholesterol and inflammation, suggesting that the same bacteria that cause gum disease also promotes heart disease.

A large study, involving 3,690 older adults, has found that drugs with strong anticholinergic effects cause memory and cognitive impairment when taken continuously for a mere two months.

A new study adds to growing evidence of a link between sleep problems and Alzheimer’s. The interesting thing is that this association – between sleep apnea and Alzheimer’s biomarkers — wasn’t revealed until the data was separated out according to BMI.

Family caregivers of dementia sufferers who are reluctant to use adult day care services might like to note the findings of a telephone survey. The study involved eight daily telephone interviews on consecutive days with 173 family caregivers who use an ADS on some days.

Last year, a cancer drug, Bexarotene, was touted as a potential treatment for Alzheimer’s disease. However, four independent studies have now failed to replicate the most dramatic result of the original study: a claim that the drug could clear half the amyloid plaques in a mere 72 hours.

I’ve been happily generous with cinnamon on my breakfast ever since the first hints came out that cinnamon might help protect against Alzheimer’s (it’s not like it’s an ordeal to add cinnamon!). Now a new study has revealed why.

Late-life depression is associated with an increased risk for all-cause dementia, Alzheimer’s disease, and, most predominantly,

Because long-term cognitive decline can occur in some older adults after undergoing surgery, there has been some concern that exposure to anesthesia may be associated with increased dementia risk.

Pages

Subscribe to Latest newsSubscribe to Latest newsSubscribe to Latest health newsSubscribe to Latest news