Can Stem Cells Be Used To Treat Alzheimer's Disease?

Alzheimer’s Disease (AD) is one of the most devastating illnesses that the human race has ever faced. It literally destroys the brain, which shrinks as a result over time. The toll of AD is not only measured in hundreds of billions of dollars in health care.

costs and millions of deaths, but also in personal and family tragedy that comes with the severe loss of memory that accompanies it.

Remarkably, scientists and doctors are getting good at predicting who has pre-clinical AD or who will ultimately get AD before patients are even symptomatic. But is knowing of any good if we can’t do much about it?

How can AD be prevented, delayed, or treated? The simple answer is that nobody really knows.

There are three key possible approaches to using stem cells to treat AD.

1) One avenue is to use stem cells to regenerate or literally regrow diseased parts of the brain. This is what people most commonly think of when they conceive of treating AD with stem cells. The problem with this approach is that the architecture of the brain is physically integral to memory so even if we could grow a fresh, young part of the brain to replace one ravaged by AD, there would be no memories there. It would be like wiping the plate clean. In theory perhaps the person could make new memories going forward in life that could be remembered or they could be re-educated, but this is not what most people imagine as a successful treatment for AD.

2) Another approach is to use stem cells such as mesenchymal stem cells (MSC) not as rebuilding agents, but rather as healers of the existing brain parenchyma. In this way of thinking,  MSC could heal rather than replace neurons for example. MSC are kind of akin to the natural doctors of the body and could have anti-inflammatory and other powers that might ameliorate AD.

3) A third concept is using stem cells such as MSC as drug delivery agents. So for example, instead of giving Crenezumab or some other drug systemically, it is possible that stem cells could directly deliver the drug within the brain from cell-to-cell far more effectively. Orders of magnitude more effectively.

Some of these same kinds of approaches might be applicable to other diseases as well.

Necotine could act as a Gateway drug

                                                                                                                GATEWAY DRUGS

According to the National Institute of Drug Abuse (NIDA), part of the National Institute of Health, scientists have identified a biological mechanism in a landmark study in mice, which could provide insight into how tobacco products could act as gateway drugs, and therefore increase the risk of abusing cocaine and perhaps also other drugs. The study, published in today's Science Translational Medicine is the first study that shows that nicotine might prime the brain to enhance the behavioral effects of cocaine. 



Researchers based their gateway drug model on epidemiological evidence on reports of most illicit drug users who state they used tobacco products or alcohol before using illicit drugs. Over the years, this model has generated substantial controversy, mainly over whether prior drug exposure to nicotine, alcohol or marijuana is causally associated with later drug abuse. Until recently, scientists have not been able to demonstrate a biological mechanism whereby nicotine exposure could increase vulnerability to illicit drug use.

In the new study researchers at Columbia University in New York City administered nicotine to mice's drinking water for a minimum of seven days and discovered they displayed an increased response to cocaine. This priming effect was based on the nicotine's effect on gene expression that was previously not recognized; Nicotine changes the structure of the tightly packaged DNA molecule and reprograms expression patterns of specific genes, in particular that of the FosB gene, which has been associated with addiction, and ultimately changes the behavioral response to cocaine. 



The researchers wanted to assess if their study results paralleled findings in humans by re-examining statistics from the 2003 National Epidemiological Study of Alcohol Related Consequences. It enabled them to investigate the link between onset of nicotine use and degree of cocaine dependence where they discovered that the rate of cocaine dependence was higher among cocaine users who smoked prior to starting cocaine compared with those who tried cocaine prior to smoking.

If the outcome in mice would display similar effects in humans, the researchers suggest, that effective smoking prevention efforts would not just prevent negative health consequences linked to smoking but could also lower the risk of progression and addiction to cocaine and possibly other illicit drug use. Researchers continue to use the mouse model to provide a new mechanism to investigate the gateway theory from a biological perspective.