Alzheimer’s Dementia Research; We’re Throwing Money Away

Much like the cancer scenario, it seems like dementia research is throwing money around looking for a “cure” for Alzheimer’s dementia.  I have said for years now that they ain’t going to find it.

By the time that someone is diagnosed with a neurodegenerative disorder, it is likely that he or she has already lost a large chunk of the dopaminergic cells of the substantia nigra (Parkinson’s) or the cells of the hippocampal region and the neocortex (Alzheimer’s dementia).  In these patients, the loss of brain cells has been going on for decades.  The process is a freight train going.  I do not think we will ever be able to stop this freight train.  Slow it down maybe:  studies on coenzyme Q10, magnesium, exercise and ginko biloba have demonstrated the ability to slow the progression of neurodegenerative disorders.

The likelihood of being able to prevent Alzheimer’s dementia, on the other hand, is very strongly supported by the medical research.  While preventative measures are beyond the scope of this blog article, you can read through previous articles by clicking here.

But, much like every other chronic disease, the prevention of Alzheimer’s dementia is not sexy.  No one gets emotional over prevention.  We get emotional over miraculous cures and amazing research discoveries.  And when we get emotional, we take out our checkbooks and give money to those groups touting research for a cure.

Most of this research on a cure has focused on the abnormal proteins found in Alzheimer’s dementia victims:  amyloid plaques (AP) and neurofibrillary tangles (NFT).  While I view these two proteins as the collateral damage that occurs in the brains of Alzheimer’s dementia patients, researchers have focused on these proteins being the cause of Alzheimer’s dementia.  The thought process is that, if we can destroy these proteins, these patients will improve.  As expected, research along this pathway continues to fail.  In someone who has been given a diagnosis of Parkinson’s or Alzheimer’s dementia, the barn door was opened a long, long time ago.

This particular study is yet another reason why we need to stop spending money on a “cure.”  In this article, researchers tried to block the consequences of a molecule called AGE, or advanced glycation end-products (specifically, the drug in question was designed to block the receptor for AGE, otherwise known as RAGE).  AGEs basically come from the diabetic process.  If you’ve ever had your HbA1c checked in blood work (and you probably have) you have had one aspect of AGEs checked.

Basically, when blood sugar levels go up, they irreversibly damage proteins.  Everywhere.  This is why the diabetic process is so darn dangerous to us–every protein in your body is destroyed by the climbing blood sugar.  Kidney proteins, muscle proteins, heart proteins, brain proteins.

Because of this, the idea was that, if we could block AGEs from doing damage, we could protect the brains of those with Alzheimer’s dementia.  Here are the specifics:

  • There were 399 participants in the trial given either a high or low dose of the drug in question.
  • Halfway through the study, it was found that those on the high dose had more confusion, falls, and greater cognitive decline.
  • As a result the study was halted.  Luckily, there were no safety concerns in the low-dose group.

In summary, it was not a good idea.  Given that we know SO MUCH about how to prevent dementia, I just don’t understand why we don’t shunt more of this wasted research money into educating the general public about prevention.  Maybe it really is as simple as prevention not being “sexy.”  Maybe we should dress it up in a little black dress and heels…


James Bogash

For more than a decade, Dr. Bogash has stayed current with the medical literature as it relates to physiology, disease prevention and disease management. He uses his knowledge to educate patients, the community and cyberspace on the best way to avoid and / or manage chronic diseases using lifestyle and targeted supplementation.