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A New Suspect In Alzheimer’s Disease Appears To Be Insulin

Recently Johnson and Johnson announced that they would be halting a clinical trial on one of their new Alzheimer’s drugs after concern of a safety issue.1

This recent failed attempt is yet another large, costly clinical trial that has shown no ability to treat Alzheimer’s disease.2 

And the mounting list of failed trials has some experts wondering if we’re looking in the wrong place for the true cause of Alzheimer’s.

German doctor Alois Alzheimer was the first to analyze the disease and made note of strange changes, noticeable in the brain of a patient who died of the disease. 

Dr. Alzheimer went on to identify two specific protein aggregates found in those with Alzheimer’s that are not present in younger brains. 

One is a plaque found in-between brain cells and the other are tangles found inside the brain cells themselves. 

Researchers later identified these proteins as amyloid and tau. 

However, what each of these structures actually does to the brain is still not fully understood. 

Dr. Alzheimer Dire Warning

During his research Dr. Alzheimer advised other scientists not to jump to the conclusion that these proteins are in fact the cause of the disease. Unfortunately, researchers quickly ignored his warning, instead over the years it has become the primary focus and researchers have assumed that the build-up of these proteins is the cause of Alzheimer’s disease. 

One of the biggest problems facing researchers is that it is impossible to test the theory in a scientific experiment. 

Just recently, new technology has made it possible to actually test what these proteins do, and so far, it isn’t what scientists expected. 

For one, mice who have ben genetically engineered to accumulate the amyloid protein in their brains, show only mild impairment.3 

Unfortunately, most drug makers have continued down the path of trying to alleviate amyloid proteins and this has been their mission from the beginning. 

The chief aim for all of these drugs is to simply decrease the levels of amyloid proteins in the brain, by either slowing down their formation or removing it altogether. And both approaches have been tested over and over again with a variety of drugs.

Yet, not one of these trials has shown any effect, and some of the larger drug companies, including Pfizer, have given up on this area of research completely.4

The enormous number of failures in this area of research has led many to believe that the amyloid protein may not be the cause at all. 

And some drug companies have changed their focus to the tau protein. 

But once again, the drug companies are putting their focus on a single protein.  

Promising New Discoveries

Many experts think that it may be necessary to rethink the cause of Alzheimer’s altogether.

One alternative theory is that it may be genetic and that certain genes may increase the risk of the disease. The biggest challenge however is that there are a relatively small total number of these genes and they are quite rare.5

Add to that the fact that earlier research suggests that Alzheimer’s does not appear to be driven by genes, so this approach does appear to be gaining ground.

Another potential avenue is to look at the risk factors associated with Alzheimer’s. And one of the biggest risk factors is type 2 diabetes.6

So, what’s the connection?

In diabetes, it’s insulin that becomes ineffective at controlling blood sugar. But there is a lot more that insulin does beside just controlling blood sugar. It’s also what’s called a growth factor and brain cells are very dependent on growth factors. In fact, if they don’t get enough they die.

When insulin growth factors are lost, neurons in the brain appear to become more vulnerable to stress. Their loss also reduces the brain’s ability to repair damage. It’s important to note that neurons live as long as we do, so damage accrues throughout your lifetime. 

When researchers evaluated brain tissue taken from deceased Alzheimer’s patients, they discovered that insulin lost its ability to act as a growth factor even in people who didn’t have diabetes.7

This has led researchers to consider the fact that certain diabetic drugs may in fact be used to fight Alzheimer’s.

In some animal studies and in recent clinical trials that are underway, this has shown promise.8  

In several studies using animal models for another neurodegenerative disorder, Parkinson’s disease, the results have also been impressive.

And in two clinical trials involving Parkinson’s patients the results were encouraging.9

In one of the studies which was a pilot study, the Parkinson’s patients who received the diabetic drugs were stable for two years. The control group who received the standard treatment protocol showed significant deterioration. 

In the other trial, which was larger and utilized a placebo group the results were confirmed. The group receiving the diabetic drug remained stable for the entire 12 months of the study.

The fact the researchers were able to see any protective benefits at all during the clinical trial is something new and supports the idea that Alzheimer’s disease and Parkinson’s disease are somewhat associated with a lack of growth factors in the brain. 

This new way of thinking about Alzheimer’s brings a refreshing and promising new angle to this devastating disease and increases the likelihood that an effective drug treatment can soon be developed.

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References:

1. McKee, Selina. "Janssen Pulls Plug On Alzheimer’S Candidate - Pharmatimes." Pharmatimes.com. N.p., 2018.

2. Anderson, James. "What Are Clinical Trials?." ReliaWire. N.p., 2012.

3. Sasaguri, Hiroki et al. "APP Mouse Models For Alzheimer's Disease Preclinical Studies." The EMBO Journal 36.17 (2017): 2473-2487.

4. "Pfizer Ends Research For New Alzheimer's, Parkinson's Drugs." U.K.. N.p., 2018.

5. Guerreiro, Rita, and John Hardy. "Genetics Of Alzheimer’S Disease." Neurotherapeutics 11.4 (2014): 732-737.

6. Mayeux, R., and Y. Stern. "Epidemiology Of Alzheimer Disease." Cold Spring Harbor Perspectives in Medicine 2.8 (2012): a006239-a006239.

7. Talbot, Konrad et al. "Demonstrated Brain Insulin Resistance In Alzheimer’S Disease Patients Is Associated With IGF-1 Resistance, IRS-1 Dysregulation, And Cognitive Decline." Journal of Clinical Investigation 122.4 (2012): 1316-1338.

8. Hölscher, Christian. "Novel Dual GLP-1/GIP Receptor Agonists Show Neuroprotective Effects In Alzheimer's And Parkinson's Disease Models." Neuropharmacology (2018): n. pag.

9. Aviles-Olmos, Iciar et al. "Motor And Cognitive Advantages Persist 12 Months After Exenatide Exposure In Parkinson’S Disease." Journal of Parkinson's Disease 4.3 (2015): 337-344.

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