The brain activity of the AD gene carrier

It’s in the genes. And the gene variant is called APOE-4. I am referring to the neurodegenerative disease Alzheimer’s disease (AD), the most common cause of dementia.

And even in early adulthood, this gene variant can already cause some structural and functional changes in the brain that is visible to the experts long before the symptoms become evident.

Researchers from the University of Oxford and Imperial College London have observed changes in the brain activity of healthy people carrying the APOE-4 gene variant. The variant is found in about 1 in every 4 people. Not every carrier will develop AD but those who have inherited one copy from their parents have 4 times higher risk for AD. Those who have inherited 2 copies have 10 times higher risk for AD compared to non-carriers.

Using the functional Magnetic Resonance Imaging (fMRI) technique, the researchers were able to distinguish difference patterns of brain activity between carriers and non-carriers. Specifically, the part of the brain involved in memory, the hippocampus, is shown to be hyperactive in APOE-4 carriers.

According to researcher Dr Christian Beckmann

“Our brains are always active – our minds wander even when we’re not carrying out specific tasks. We were surprised to see that even when the volunteers carrying APOE4 weren’t being asked to do anything, you could see the memory part of the brain working harder than it was in the other volunteers. Not all APOE4 carriers go on to develop Alzheimer’s, but it would make sense if in some people, the memory part of the brain effectively becomes exhausted from overwork and this contributes to the disease. This theory is supported by studies that have found the opposite pattern in people who have developed Alzheimer’s, with these people showing less activity than normal in the memory part of the brain.”

Similar findings have been reported by researchers at the Medical College of Wisconsin. Again using fMRI, the American researchers investigated the function of the hippocampus and the posterior cingulated cortex. These two brain structures are important for memory processing, especially information acquisition, filtering and sorting.

Offsprings of AD patients who are symptomless but nevertheless carry the APOE-4 gene variant exhibited significantly reduced (35% less) functional brain connectivity between the two previously mentioned brain structures.

The genetics behind AD is slowly becoming clear. So is the link between the gene variant and brain functioning. However, what still needs to be clarified is why some APOE-4 carriers develop full blown AD and some don’t. Surely it cannot be ruled out that environmental factors (e.g. lifestyle) may play a role.

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