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Research: Current Research
   
 

Report on Deep Brain Stimulation

In this section:
Introduction
Research Advances from ICAD
Report: Enhancing Quality of Life for People Living with Dementia
Response to study on caffeine as a viable treatment for Alzheimer's disease
Lowering dementia risk in women
Conference on Clinical Trials on Alzheimer's Disease
Ginkgo biloba study
An Update on Stem Cell Research
Health Canada Approval of Exelon™ Patch
A Report on Alzheimer's Disease and Current Research
Report on Deep Brain Stimulation
Report on Enbrel Study
Comment on Beta-Amyloid
Use of Vaccines for Treating Alzheimer's Disease
Report on Dimebon

By Dr. Jack Diamond, Scientific Director, Alzheimer Society of Canada

The report

The report describes an unexpected outcome of an operation intended to help reverse a long-standing obesity in a 50-year-old man. A tiny electrical device was inserted into a deep region of the brain called the hypothalamus, a region involved in a number of functions which include the control of appetite. The intent was to electrically stimulate nerve cells (neurons) located there which cause release of hormones that act back on the brain to suppress appetite. The desired outcome would of course be a long-term one (a sustained loss of appetite). What happened in this patient, however, was a relatively immediate event that occurred during the electrical treatment.

The patient suddenly reported that he was remembering a long-ago (some 30 years) event, and as the intensity of the electrical stimulus was increased, so did the details of the memory. Earlier findings by the great Dr Wilder Penfield who founded and made famous the Montreal Neurological Institute (MNI) showed that quite superficial stimulation of the exposed brain (almost always of patients with epilepsy) could on occasions evoke seemingly long-term memories, although these were not firmly established as such.

In the new study, the electrical stimulation was applied to deep brain structures. The investigators satisfied themselves that the nerve messages they were initiating locally spread by way of the existing brain circuitry to other brain regions; among those regions were those involved in memory and emotions. Presumably it was the activation of those regions that evoked the patient's memories and feelings.

Interestingly, over the following year, the present patient's memory and thinking appeared to improve, but this was only apparent if periodic electrical stimulation was given through the electrical device, which stayed buried in his brain (this involved the use of a pacemaker implanted near his collarbone).

Now, it is important to remember that there was nothing especially wrong with this patient's memory. As in all of us, memories lie buried that might never be recalled under normal circumstances. But the memories are there, and these studies revealed a possible way to access them utilizing existing circuitry, though of course this would be a random process.

Can these findings be used to help recover lost memories in Alzheimer patients?

The same Toronto team have now implanted the device into six patients with Alzheimer's disease to see whether the stimulating procedure is acceptable and safe, and if it releases memories locked away by the disease. It's mentioned that there may already be indications of some memory improvement.

The problem in extending this thinking to the person with Alzheimer's disease is that here we are dealing with significant loss of nerve cells – hugely more than may occur even in the most elderly person without dementia. So the key question is – have the long-term memories gone because brain cells critical to the storage of those memories have gone? Or – is the problem that the memories are still there, but cannot be accessed because critical connections have been lost when other cells died?

There is some encouraging news in this regard. The first comes from mouse studies in which brain cells were destroyed by activating certain genes. The mice then had a poor memory-forming capacity, and experimentally-induced long-term memories disappeared. These mice were then put into an enriched environment of the sort that in normal mice significantly improved both memory-forming capacity and cognitive functions, and also was shown to enhance connectivity between brain neurons.

The result? The mice with the brain cell loss but exposed to an enriched environment improved their memories – and recalled the long-term memories! The explanation offered was that the enriched environment sufficiently enhanced connectivity among surviving brain neurons as to now enable access to surviving neurons associated with memory storage. Now these were not Alzheimer mouse models, admittedly. But the findings certainly support the notion that long-term memories may not necessarily be lost when nerve cells die, but may simply become inaccessible, at least until the disease reaches advanced stages.

The second news is highly anecdotal, but necessarily so. This is a not infrequent observation of family members and caregivers who have chosen to interact, sometimes for years, with their loved ones who have Alzheimer's disease as though they could hear and see and understand everything, but simply had lost the ability to communicate or express their awareness or feelings. The observation made was a totally unexpected return, evidenced by a casual remark, of an awareness by the affected person of what was going on, and who they were with. So heartening to the family!
Although the specialized neurosurgical procedures used in this new report make it unlikely that the treatment afforded this patient could ever become a routine one with Alzheimer patients, more knowledge about it will be required even if its use is to be contemplated for selected cases. The most needed finding is that it can work in a person with Alzheimer's disease whose long-term memory has virtually disappeared. This would be such an exciting result! Moreover, it would stimulate further research into how vanished long-term memories can become accessible, using either appropriate drugs or non-invasive behavioural training strategies.

So – we wish the Toronto group luck in their continuing endeavors to confirm their findings, and to extend them to people with Alzheimer's disease.

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This page last reviewed/revised February 2008.
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