Scientists have been trying to figure out how memory works for over a century. There is huge potential for such research to direct drug design for Alzheimers disease and other conditions involving memory loss.
There is no known cure for Alzheimers disease.
What is Alzheimers disease?
In Alzheimers, brain proteins form abnormal plaques and tangles, resulting in the death of brain cells and loss of memory. The protein changes are associated with a shortage of neurotransmitters, chemicals that convey messages between cells.
These neurotransmitters are very important and can be considered the ‘words’ of brain language.
The lack of neurotransmitter is addressed by drugs that treat symptoms of Alzheimers. One of these scarce neurotransmitters is acetylcholine. Several drugs focus on boosting existing levels of acetylcholine to address this chemical shortage.
Other drugs attempt to prevent further entrance of calcium into the brain. Excess calcium in brain cells damages them and causes a break-down in communication with other brain cells.
One of the challenges to understanding memory- and the brain in general- is that a mammal is estimated to have 1011 (100 billion) brain cells.
In a human, each of these neural (brain) cells is estimated to connect to 1000 other cells, meaning there are 1014 (100 000 billion) interconnections. These cell connections are called synapses and are structures that transmit chemical signals between cells. This communication involves a chemical neurotransmitter and specific regions of different calcium concentrations.
There has been much study done to begin unravelling the memory mystery.
“Memory is produced when two neural cells interact in a way that somehow strengthens future signalling through the synapse.”
Donald O. Hebb, Canadian psychologist, 1949
Following on from Hebb’s research, in 2007 Professor Joe Z. Tsien reported that a protein complex known as the NMDA receptor is responsible for strengthening future interaction between two neural cells. His research involved genetically engineering mice with no NMDA receptor and mice with enhanced production of the NMDA receptor. The mice with more NMDA receptors ‘learned faster and retained memories longer than unaltered mice did.’ He concluded that activation and reactivation of this NMDA receptor links memory from the molecular to the network level.
In 2009 further research was reported by Kenneth S. Kosik, a neuroscientist at the University of California Santa Barbara. He explained the strengthening of the synapse (join between two neural cells) as being the result of protein production. Proteins build the connection between brain cells and make it stronger.
Kosik found that the production of new proteins can only occur when a ‘silencing complex’ is turned off. When synapses are activated, one of the proteins wrapped around the silencing complex gets degraded. This allows the cell to start making these proteins to strengthen the neural connections.
Kosik was able to observe some of the specific proteins involved in building memory connections between brain cells.
The strength of neural synapse connections is important but short-lived. Synaptic long-term memories are encoded at a deeper molecular scale. The enzyme CAMKII (Calcium/calmodulin-dependent protein kinase II) has long been recognised as a major player in long-term memory production.
In 2012 a group of scientists from the Universities of Alberta and Arizona looked at long-term memory coding using molecular modelling. They showed a spatial connection between microtubules and the enzyme CAMKII. Microtubules are major parts of the structural cytoskeleton within brain cells.
This group, including physicists Travis Craddock and Jack Tuszynski and anesthesiologist Stuart Hameroff, have demonstrated a mechanism for encoding synaptic memory into microtubules. They believe that memory is written into the cytoskeleton of brain cells.
There is on-going research aimed at untangling the mystery of memory formation and retention. Science is not yet in a postition to try to prevent Alzheimers or memory loss, but greater understanding of how memory works will help design drugs to that do this.
It is worth noting that there are ethical implications to understanding the formation of memory in the brain. As soon as science understands something, it tends to replicate it.
Memory from Mind to Molecules, Larry R Squire and Eric R. Kandel, (2000) Scientific American Library, USA
NZ Alzheimers Society website: http://www.alzheimers.org.nz/assets/Resources/Alzheimers-disease.pdf
How the Brain encodes memories, The Hindustan Times [New Delhi] 24 Dec 2009
Brain memory code cracked, Asian News International [New Delhi] 20 Mar 2012
The Memory, Scientific American July 2007