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The Wisdom of Psychopaths
In this engrossing journey into the lives of psychopaths and their infamously crafty behaviors, the renowned psychologist Kevin Dutton reveals that there is a...
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Scientists have found that a lessened supply of new nerve cells in the adult brain apparently triggers short-term memory loss typically associated with aging, setting the stage for one day developing therapies designed to maintain a steady supply of fresh neurons to keep the mind sharp.
"Neurogenesis (nerve-cell production) goes down with age … it's known that with old age there's a decrease in short- term memory," says Ronald Evans, a genetics professor at the Salk Institute for Biological Studies in La Jolla, Calif. "We know that if we can increase the process, we know what the consequence could be in the brain, which would be to increase short-term learning and memory."
"New experiences, new memories [and] new learning [are] greatly facilitated by neurogenesis," he adds. "Neurogenesis is in fact a fundamental feature of learning and memory. … Neurogenesis goes down with age; and, it's known that with old age there's a decrease in short-term memory."
Evans is co-author of a study published in Nature that shows impaired short-term memory and learning in adult mice, in which scientists blocked the process of neurogenesis. They did this by engineering mice that lacked one copy of the gene responsible for the production of Tlx, a protein that the team had previously determined was crucial to maintaining and renewing the arsenal of neural stem cells.
"The other allele (gene copy) is normal, but it is susceptible to knockout upon ingestion of [the] orally active estrogen antagonist" tamoxifen, Evans says. "It's a very effective knockdown." After being given tamoxifen (perhaps best known as a breast cancer drug) for eight days, an otherwise normally developing mouse had more than 80 percent fewer new neural stem cells in its hippocampus (a structure in the brain's frontal region linked to short-term memory).
The genetically altered mice performed as well as normal peers did in experiments based on learning out of fear, such as associating a sound or light flash with a shock to a paw. They failed, however, to perform up to speed on a spatial memory task: It took days for the mice lacking new nerve cells to lessen the time it took for them to find a platform floating in a pool of opaque liquid on which they could stand.
Normal mice took about three days to make the connection, but Evans says the knockout mice were still on "a learning curve" six days into the experiment." They eventually learn," he says, "but it takes them much longer."
Martin Wojtowicz, a physiologist at the University of Toronto, downplayed the finding, noting that it contradicts his own research on rats, which found a link between neurogenesis and fear, but not memory. "They see a very subtle effect in the water maze," he says, "but other than that, nothing."
Evans, however, sticks by the team's conclusions, pointing out that Nature required several additional tests be conducted to verify the data. He also notes that in previous studies, researchers irradiated parts of the animals' brains or injected them with cancer drugs that destroyed more than targeted nerve cells, making it difficult to determine whether it was the suspect cells or other damaged areas that were to blame for certain behaviors. In contrast, he says, his team explicitly links neurogenesis to short-term memory, which in the future could lead to a drug designed to stimulate nerve cell production and potentially counter memory loss in older adults.
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9 Comments
Add CommentWhat about hydergine? It may mimic nerve growth factor. Sold over the counter in Europe and most of the world outside North America, it has only rare problems with perhaps triggering psychotic episodes in people prone to psychosis.
Reply | Report Abuse | Link to thisThe compound resveratrol has shown interesting neuroprotective properties in clinical trials. Drs. Anderson and Setia reported in a January paper that of 121 with memory loss and early Alzheimers symptoms patients given biotivia Transmax, an extract of red wine used by researchers, 94 showed marked improvement in cholesterol levels, reduced inflammation and improved circulation. Resveratrol works by activating the human Sirt 1,2,3 genes much like caloric restriction does. Sirtris pharma is developing a synthetic version of transmax which it intends to have on the market in five years. In another study by Dr. Sinclair of Harvard published in the journal Nature in November transmax was shown to increase the life span of obese mammals by 31%. This is an exciting area of research and could lead to some revolutionary new preventative strategies and safer less invasive treatments for heart disease. I Dr. Sinclair's study of obese mice he found that those fed resveratrol lived 31% longer and were free of cardiovascular diseases.
Reply | Report Abuse | Link to thisI want to report some personal experience which might show that other approaches may exist to look for causes to the loss of short-term memory, and to which degree it may be reversible.
Reply | Report Abuse | Link to thisI am in the early sixties, a scientist trained in thorough observation. I have been going through an episode of moderate to severe depression and take two prescription drugs.
About two months ago I experienced a sudden impairment of short-term memory. The phenomenon was quite selective, and did not affect my capability to perform complex tasks (if and when I find the energy).
The impairment of short-term memory became prevalent in simple tasks. Making coffee, e.g, should be straightforward: Take water, filter, coffee, and press the switch. But this did require more attention than available, and I forgot in between these steps, which I had made. So I omitted or duplicated one or the other (with funny results), or I forgot that I am in the process of making coffee.
(part 1 of 3)
When I needed something from another room and arrived there seconds later, I frequently could not remember for which item I had come, even more than once for the same item.
Reply | Report Abuse | Link to thisI am aware hat something like that is familiar to everyone of us ("Now, did I put sugar into my coffee already or not?"), but frequency and severity was outstanding.
One most funny example: I went to the bathroom for a shave. I found myself looking into the mirror day-dreaming, and remembered why I was in the bathroom. So I poured preshave on my hand and put it to my face, and was surprised when my skin was perfectly smooth. Even with this clue I could not remember anything of a shave immediately before.
Now the key observation: Parallel to alterations in the severity of other symptoms, the impairment of short-term memory was (and still is?) more or less pronounced. On "bright days" I might not become aware of it at all, on "foggy days" it reached its very extreme.
(part 2 of 3)
I believe that no direct link exists between blood concentrations of one of the drugs and the symptom I am writing about, as my compliance is good.
Reply | Report Abuse | Link to thisTherefore I conclude that one of the drugs affects short-term memory in a way that it becomes sensitive to intrinsic alterations in receptor activity.
My interpretation so far is that short-term memory can be induced by a (i.e., at least one) prescription drug and appears to be reversible when initiated that way.
Is there some indication in the literature that such a phenomenon is shared by more patients and how it is being triggered in them?
Any result of literature search and questioning of patients could help elucidating the mechanism and lead to a non-clinical model more close to clinical experience.
A lead to a new class of compounds blocking a step in the mechanism leading to loss of short-term memory (or repairing a malfunction) might appear.
Please excuse the length of my posting.
(part 3 of 3)
After some rest I found a more concise conclusion of my rambling commen
Reply | Report Abuse | Link to this"Short-term memory loss could have an alternative and/or additional cause besides defects on the cellular level.
With my observation I wanted to illustrate that changes on the receptor level may have an effect as well."
A question I am puzzle with: when we speak of loss or decline of memory are we not confusing the aspect of memory that has a meaning and facilitate or participate (consciously or unconsciously) the task we are performing at the time, with the physical means or cellular structure involved?
Reply | Report Abuse | Link to thisI dont deny that there might be strict correspondence between the correct performing of the physical aspect involved with the memory and its usefulness and adequacy to the task, but to me the correspondence would be the same as between a person that drives a car to the one that drives a bicycle, or when they both drive through a paved or unpaved road.
I found it difficult to consider that a memory can be lost, or declined, (unless we are facing a pathology) I am more inclined to consider the memory as whole; (and remaining always so) and not a cumulus of separate parts that can be lost here and there.
Am I so wrong?
Is this "knockdown" reversible when tamoxifen is not given?
Reply | Report Abuse | Link to thisIs the "knockdown" reversible once tamoxifen is eliminated?
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