Dr Pierre-Marie Lledo from the Pasteur Institute in Paris reported on his studies of the sensory neurones in the human olfactory (smell) system. (Neurones are electrically excitable cells in the nervous system that process and transmit information.)

Sensory neurones are replaced every two months. The brain, whose neurones are also regularly replaced, is the first relay of
olfactory information.

‘New-born’ neurones come from stem cells, after which they have to ‘migrate’ to the site in which they are needed and then ‘integrate’ themselves with the existing network. This process takes around four weeks during which time the neurone is not able to ‘speak’ or transmit information but is able to ‘listen’ or receive it. The information which the neurone receives may alter it or allow it to be ‘epigenetically regulated’. (This means that although the neurone is genetically programmed, it can be altered by its ‘experiences’ on its way to being integrated into the network.)

Moreover, this regulation can be controlled. For example, olfaction has a strong link to memory. The more the sense of smell is used the more new and more complex ‘smell cells’ will be created. Mice introduced to new smells every day for 40 days doubled the number of cells created every day and improved their short-term memory from 30 minutes to four hours.

Is it possible to adapt and use new born neurones? We don’t know whether using stem cells or stem cell neurones devised for olfaction for some other purpose might throw the whole system.

Dr Tom Brenna from Cornell University, Ithaca looked in more detail at DHA (docosahexaenoic acid) the highly unsaturated fatty acid that is vital for efficient brain function.

The human brain continues to accumulate DHA for up to two years although it accumulates most rapidly in the last three months of pregnancy. The brain continues to grow and refine its synapses
(connection or signalling points) throughout early childhood.
Supplementation of breast-fed babies with DHA resulted in significant improvement in visual acuity. It also appears that regular fish eaters (who absorb high levels of DHA from the fish) are 50% less likely to suffer from Alzheimer's.

Dr Stephen Cunnane from the Université de Sherbrooke, Canada looked at brain function in the aging. In Europe 10% of over 65 year olds suffer from cognitive brain decline, as do 50% over over 85 year olds.

Genetic factors may be relevant in this decline but they are uncontrollable. However it seems clear that insulin resistance/type 2 diabetes, low fish intake and a reduced uptake of glucose (brain fuel) all affect the incidence of decline.

To keep all neurones and synapses in the brain fully operational requires a high input of fuel (glucose and metabolites - amino acids, glycerol and glycogen): it takes 74% of the total energy consumed by a new born baby, 23% of total energy consumed by an adult.

In omega 3 deficient animals the brain uptake of glucose is poor; there is 20% less glucose uptake in the brains of Alzheimer's patients than in normal brains. Is there a connection?
Insulin must play a role in glucose supply so insulin resistance impairs the ability to get glucose into the tissues, thus starving the brain of fuel.

It is possible that ketones (the substances made when the body, in search of energy/fuel/glucose, breaks downs fats to access it) may help to supply the brain with fuel but there is little evidence of this.
It is not clear whether the inability of the brain to access sufficient fuel is a vascular problem (not enough glucose is getting through) or neurone problem (they are unable to capture the glucose when it arrives). Nor is it known how fatty acids are actually transported into the brain.

Humans are not good at making DHA out of omega 3 fatty acids - we are most efficient as neo-nates but get worse as we get older. But if there is a sufficient dietary supply (fish) there is no need for us to convert it anyhow.

Dr Fernando Gomez-Pinilla of the University of California, LA discussed the studies he had undertaken with rats on fitness training and cognitive decline.

Increased exercise in rat models was shown to increase their hippocampal levels of BDNF - brain-derived neurotrophic factor. BDNF is a protein that supports existing neurones, and encourages the growth of new neurones and synapses in the hippocampus, cortex, and basal forebrain - areas vital to learning, memory, and higher thinking. Increased exercise enabled the rats to learn faster and to recover more quickly from a traumatic brain injury.

It was also found that a diet high in saturated fats reduced
hippocampal levels of BDNF while supplementing with fish oils increased levels of BDNF. Like the exercise, the fish oil supplements speeded up recovery from traumatic brain injury. Combining exercise and good diet had a positive synergistic effect.

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