CONNECTING AND PROTECTING OUR MEMORIES
By Peggy Willocks

Memory is a highly individualized phenomena in some respects. Two people can see the same movie and remember very different scenes or facts. Memory has to be “connected” with one’s experiences. And the more connected, the easier it is to recall. In “Brain Biology: basic gardening,” Kathie F. Nunley has the following to say:

As you read the words on this page, you are utilizing thousands of the 100 billion (more or less) nerve cells that make up your brain. The electrical firings and chemical messages running between these cells, called neurons, are what produce our thoughts, feelings and interactions with the world around us.

One hundred billion neurons may seem like a lot of nerve cells, but is actually only about 20% of the number we originally start with. The number of nerve cells in our brain peaks prenatally and then they start to prune themselves out, one by one, through childhood. By the time we enter adolescence, our brain has chosen the final select neurons it will keep
throughout our adult life. The decision is based on which cells we use and which we do not. The cells we do not use are pruned away leaving more room to add branches, or dendrites, to the nerve cells that we do use. New branches are added as the brain receives and processes any new information.

New growth, on the other hand, comes in the dendrite development, or branching of well-used neurons. This branching is caused from chemicals known as Neurotrophins. Neurotrophins are a group of proteins which are responsible for the growth and development of neurons. As you may suspect, we use a lot of neurotrophins during childhood as the brain has massive growth and development. But we continue to use neurotrophins all of our lives, especially in the hippocampus area, the brain region responsible for new learning and new memory formation.

There are many neurotrophins at work in the brain. The first one discovered is known as NGF (nerve growth factor). Others, discovered since, have equally self-explanatory names as brain derived neurotrophic factor (bFGF), and glial cell-line derived neurotropic factor (GDNF). These neurotrophins work by attaching themselves to receptor sites on nerve cells and causing the cell membrane to change shape, grow and branch. . . . it is thought that the majority of neurotrophic work is also done during sleep, especially the non-REM cycles of sleep. A study by Marcos Frank and Michael Stryker, at UC San Francisco, in 2001, showed the tremendous amount of branching and subsequent learning that took place during sleep (paraphrased). While most of the science community historically considered that the REM, or dreaming cycle of sleep was the time when most wiring took place, Stryker’s work and the research following that study continue to show that it is actually the non-REM cycles that help hard wire in the information learned the previous day. Therefore . . . we MUST get sufficient sleep following the learning of new information if we want that information stored in a long-term, complex network of neuron branches.

The cortex of the brain begins operating at adult activity levels by age 4. Additionally, by age 4 a child’s brain is more than twice as active as is an adult’s (so THAT’S why older folks can’t remember! ). In comparing the adult brain with a child’s brain, we find that the child’s brain burns much more glucose. There’s a reason for this - the child’s brain must maintain trillions of connections between neurons, more than twice as many as eventually are retained. Consumption of glucose continues at a feverish rate through age 10 and then slows down. Until about age 16, glucose consumption continues in the fast lane. Then it levels off at about the same rate as the adult brain (there’s no way you can convince me that my 16-year-old had a brain like an adult!).

Way too many connections are created in the brain’s cerebral cortex, at which time we have a waiting period to decide which ones we will keep. These connections are synonymous with potential pathways that an electrical impulse may travel. Repetition strengthens these connections, and those that are not used become possible victims to elimination (the ole “use it or lose it” theory).

To demonstrate this type of “conditioning” of the brain’s pathways, try this simple experiment. Hold up a piece of typing paper. Tell the person you are going to ask a couple of questions, and they are to respond spontaneously. Ask, “What color is this paper?”; to which they will respond, “White.” Then immediately ask, “What do cows drink?” Nearly 100% of the time, the response will be, “Milk.” (Of course cows drink water, unless you’re a baby cow - which is technically a “calf.) This helps confirm that common “pathways” allow us to retrieve frequently-used information without much thought.

Now to the application of all of this to Parkinson’s (PD):

· Although many other factors are involved in determining the frequency of a Parkinson’s diagnosis with dementia (patient’s age, duration of PD, Lewy body pathology, Alzheimer’s connection, etc.), the percentage is approximately 30%. We help build our memories from the time we are born (maybe even while inutero!). If we don’t continue to make “connections” with what we learn, we reduce our memory capabilities. This may be yet another reason for such variance in frequency percentages.

· The National Institutes of Neurological Disorders and Stroke (NINDS) is currently recruiting candidates for participation in a trial for a medication to treat dementia in patient’s with Parkinson’s. The medication is Donepezil – more information can be obtained at the site below: http://www.clinicaltrials.gov/ct/show/NCT00030979?order=5

· The more you use your brain, the less the likelihood of developing dementia. This is a highly ambiguous statement and has not been fully supported by research. However, common sense and the fact that patients in situations where they do not receive as much stimuli as possible, add strong validity to this hypothesis. According to recent research, neuroscientists have identified specific "time windows" and activities that can stimulate neuronal growth in the young mind and “fitness activities” that help optimize learning and/or memory in the aging brain. This discovery of the brain's plasticity indicates that “building the brain” can take place at any age. Such treatments and strategies are actually slowing cognitive decline and improving the quality of life. (Medical Breakthroughs from the Society for Neurological Science (www.sfn.org/BAW) )

· There are a variety of tools available that can help improve memory, such as mnemonics. See this site for a myriad of suggestions: www.mindtools.com/memory

· Sleep and memory capability have a strong correlation. Sleep disorders affect up to 70 million people in the United States. This costs about $100 billion each year in accidents, medical bills and lost work. (Statistic from Brain Facts, Society for Neuroscience, 2002) People with Parkinson’s often suffer from sleep disorders (insomnia, somnolence, sleep attacks, hypersomnia, sleep apnea, vivid dreams, etc.). In an AP news report in October, 2003, the following statement was made: “It (sleep) is not just a matter of physical recharge. Researchers say sleep can rescue memories in a biological process of storing and consolidating them deep in the brain's complex circuitry.”

· Research with neurotrophins , especially glial cell-line derived neurotropic factor (GDNF), can not only move us closer to better treatment or a cure for PD, but can also have impact on memory-associated disorders (dementia, Alzheimer’s, etc.).

(See this NIH meeting summary for some recent topics of research: http://www.drugabuse.gov/MeetSum/ameetsum.html )

In conclusion we might be more responsible for our cognitive decline than our disease itself! That’s a powerful statement that leaves us with a strong charge in development and expansion of our minds during our lifetime.

(You must ask permission of the author to reprint this article in its entirety; however, single copies may be used for educational purposes and parts therein may be quoted.)

References:

“Dementia Explained: Parkinson Disease Dementia, Lewy Body Dementia, Alzheimer Disease: Are they the Same? Or Different? Does it Matter?” Lieberman, A. 6/2002 http://www.parkinson.org/dementiasame.htm

“Dementia in Parkinson’s” Lieberman, A. 4/2002 http://www.parkinson.org/pddement.htm

“Memory and executive function impairment predict dementia in Parkinson's disease“

Levy G, Jacobs DM, Tang MX, Cote LJ, Louis ED, Alfaro B, Mejia H, Stern Y, Marder K. PubMed 11/2002

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12465060&dopt=Abstract

“Brain Biology: basic gardening,” Nunley, K.A. 2002

“Dementia and Parkinson’s” Health Center.com

http://www2.health-center.com/body/illnesses/neurology/parkinson/about_parkinso/coexist.htm

“The Brain During Sleep” Neuroscience for Kids.

http://faculty.washington.edu/chudler/sleep.html

“Good Zzzzs Help Memory” CBS AP News Oct. 8, 2003

http://www.cbsnews.com/stories/2003/10/08/health/main577140.shtml