Your Memory Is In Your Blood

I was two thirds of the way to the end of a 45 member circle at a workshop, hating my position in the line-up. The facilitator started an introduction exercise that involved reciting the names of preceding individuals -from the beginning. The room was filled with science types, many commenting on the cognitive process of memory. As the people before me went, I concentrated on the names, faces and associating ideas with them. Dawn had an image of the rising sun behind her dark hair and Robin's pale blue blouse was like an egg.

The blood flowing through our veins is packed with cells -one type, platelets are small things. I imagine they're slightly squishy like a ball not quite taught with air but with the texture of a basket ball -the bumps representing lipids. In the living balls, the lipids constantly exchange, replacing each other. The enzyme responsible, phospholipase A2 (PLA2), may play a role in memory.

PLA2 is not just in the tiny platelet cells; it's in a variety of other cell types including neurons. In the brains of victims with memory deficits, PLA2 activity is decreased. With the idea that the PLA2 activity in platelets reflects that of brain cells, researchers at the University of Sao Paulo in Brazil asked whether brain training exercises could increase the activity of this enzyme in healthy elderly subjects.

The tasks researchers gave the subjects included a list recall exercise, much like the name task that I so dreaded. The experimental group was “trained” in four 90 minute sessions that included a discussion regarding memory and aging and a practice component that introduced the concept of mnemonic strategies (associating words with related meanings).

Blood was taken at the outset of the experiment and when it was over two weeks later. Researchers tested for PLA2 activity... it changed, generally increasing with the exercise. One caveat: there are several types of the enzyme. Some of them stay in the cell, while others are secreted. One of them depends on calcium and another is calcium independent. This last one, calcium-independent PLA2, decreases in patients with Alzheimer's disease. This one, however, also decreased in healthy individuals that underwent the training.

The paper concludes “the present data support the notion that cognitive training promotes biochemical changes that correlate with memory acquisition and retrieval... and illustrates the potential of non-pharmacological intervention to improve cognition in older adults through the modification of neurobiological systems.” So, learning can change your brain chemistry. And this change is likely paralleled in your blood.

With the mentioned caveat, I wrote to Dr. Wagner Gattaz, lead investigator of the study. Here is his reply:

I am also confused by this increment in iPLA2, I would expect exactly the contrary. I can not explain it. Therefore, the conclusion from our data is that cognitive training causes changes in membrane phospholiopid metabolism, in a very general manner.

1. Cognitive activity through the life, as measured by years of school, reduce the risk for AD. This is one of the most consistent findings across several studies.
2. PLA2 is low in AD
3. Cognitive activity increased PLA2
4. Thus, this finding (3) may provide a biological rationale for (1)
5. Maybe the use of cognitive training should be emphasized in individuals at risk for AD.

We are now investigating the effects of cognitive training on PLA2 in patients with AD. Our question to be tested: does the enzyme activity also increase in these patients?

After doing the naming exercise, I would love to have access to my own PLA2 levels and how they change over the course of the task, or better yet, a lifetime. Undertaking research on brain lipid biochemistry in people and trying to relate it to blood chemistry is quite the cognitive task. I wonder what Dr. Gattaz's PLA2 activity is.

TALIB, L., YASSUDA, M., ODINIZ, B., FORLENZA, O., GATTAZ, W. (2008). Cognitive training increases platelet PLA2 activity in healthy elderly subjects. Prostaglandins, Leukotrienes and Essential Fatty Acids DOI: 10.1016/j.plefa.2008.03.002