I added some information to my section "How to Find Medical and Scientific Information." The addition consisted of a new link, http://librarysearch.org, which tells you about intra-library loans and some service packed such as EBSCO (which I have separately discussed) and Illiad (which is the main interlibrary loan service). There is also some other information of general interest to those who want or need to do library research.  I also corrected a few typographical errors and reworked a few of the paragraphs in an effort to make my presentation more clear.

Limbic encephalitis is a poorly understood inflammation of the hippocampus and other parts of the limbic system that causes a subacute confusión, memory loss, seizures and, sometimes, a permanent dementia and/or death.  In many cases it seems  to be due to an autoimmune response to cancer, in which case it would  be called paraneoplastic (limbic) encephalitis.  In other cases it appears to be an idiopathic (of no known cause) autoimmune response.  A number of antigens have been identified in the autoimmune  cases including  a number of synaptic proteins such as N-methyl-d-aspartate (NMDA), α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) and gamma amino butyric acid (GABA) receptors.  A whole subgroup of limbic encephalitis has been thought to be due to antibodies not to a synaptic protein but, rather, to voltage gated potassium channels.

The authors of the Lancet Neurology article listed below challenged this connection.  They identified 57 patients who had the syndrome of limbic encephalitis and who, according to the conventional tests, had antibodies to the voltage gated K channels.  But they used definitive methods of identifying the antibodies and found that the antibodies were all directed toward LGl1, a protein secreted at the synapse which appears to facilitate synaptic function by promoting or modulating interactions between the pre synaptic and post synaptic parts of the synapse.  Thus, this category of limbic encephalitis is actually related to a synaptic protein similar to cases involving NMDA, AMPA and GABA receptors.  But it is also different from these in that LGl1 is a secreted protein, not a receptor.

http://www.thelancet.com/journals/laneur/issue/current

Investigation of LGI1 as the antigen in limbic encephalitis previously attributed to potassium channels: a case series Meizan Lai, Maartje GM Huijbers, Eric Lancaster, Francesc Graus, Luis Bataller, Rita Balice-Gordon, John K Cowell, Josep Dalmau

Lancet Neurol 2010; 9: 776–85

2010; 9: 776–85

Lancet Neurol 2010; 9: 776–85

2010; 9: 776–85

I am originally from the Chicago area and for a number of years I was on the faculty in the Neurology Department at the University of Chicago. In those days, one of the competing hospitals was Evanston Hospital, which was affiliated with Northwestern.  Also, back then, University of Chicago had a major affiliation with a superb private hospital called Michael Reese. Unfortunate economic events produced many problems which limited Michael Reese's ability to be a major academic partner of the University of Chicago.  It still exists as a part of the Envision Hospital Corporation. It's great that Envision has turned it around because it still plays an important role, particularly on the South Side of Chicago. It also appears to maintain it's status as a tertiary center incorporating teaching and research as well as medical care. I am happy about that because Michael Reese has a great tradition. But, to my knowledge, it no longer is a major University of Chicago affiliate and for a long time I have felt that University of Chicago needed another strong private major affiliate.

About a year ago I learned that Evanston Hospital was now a part of a larger system called NorthShore University Health System and, to my surprise, it is now affiliated with the University of Chicago. I think that was a great move both for Northshore and the University of Chicago. Even more recently, a new Neurology Chair, Demetrius (“Jim”) Maraganore, MD came to Northshore from Mayo Clinic where he was a Professor at the Mayo Medical School and the head of Mayo's movement disorders section. I see this as an outstanding development for neurology in the Chicago area.

The article from MedicineWorld.org, currently running to the right of this column, reports the disappointing news that there is no definite proof that any of activities presently touted as helping to prevent Alzheimer's disesase actually have any efficacy at all. Quoting from the MedicineWorld.org report, "Alzheimer's disease is a feared and heart-breaking disease," said Dr. Martha L. Daviglus, conference panel chair and professor of preventive medicine and medicine at Northwestern University, Chicago. "We wish we could tell people that taking a pill or doing a puzzle every day would prevent this terrible disease, but existing evidence doesn't support this". 

This does not surprise me. All of the stories that have come out in the press advocating excercise, mental stimulation, medication, and even coffe have been backed by very slender evidence. It never was likely that any of those items could make a major change in the biological processes leading to Alzheimer's disease.

Of course, the lack of proof of efficacy is not the same as a proof of lack of efficacy. I believe it is still possible that some of things we do in our lives could produce a small perturbation of our trek toward dementia, either positive or negative. But these small effects are going to be difficult to prove. There are some upcoming trials of medications that attempt to attack some partially understood mechanism underlying Alzheimer's disease. One such potential treatment is a gamma secretase inhibitor. Gamma secretase cuts the Alzheimer precursor protein (APP) at just the right spot so as to produce toxic amyloid fragments.  So one might think that by inhibiting this enzyme one could block the progression of Alzheimer's disease. Of course, some scientists feel that amyloid actually contributes little to Alzheimer's disease. If so, the gamma secretase inhibitors probably will have no beneficial effect.  My personal opinion is that amyloid is actually a major contiributor to Alzheimer's disease though perhaps it is not the only one. So I predict that the gamma secretase inhibitors will show a definite measureable efficacy. I doubt that such things as excercise and brain stimulation games have the capacity to help very much. But I could be wrong.