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Posted

Well, my grandmother has Alzheimer's, and after reading about it I can't really figure out why there isn't a cure for it yet. I have a general idea of what Alzheimer's is, and you could say that I'm very familiar with the symptoms.

I believe my grandmother is in the 'moderate dementia' stage (http://en.wikipedia.org/wiki/Alzheimers#Characteristics), so it's probably a little late for her but if there was a cure, how long would it take to have effect?

This obviously isn't organized very well, so I'll just write out my questions.

 

1. Why isn't there a cure? From what I've read it doesn't sound as untreatable as, say, AIDS.

 

2. If there was a cure that was administered in the pre-dementia or early dementia stage, how long would it take to 'fix' the loss of neurons?

 

3. What are the chances of me acquiring it? My great-grandmother had a very mild case, my grandmother has a very serious case, I'm not entirely sure about my mother yet. It seems to run from my mother's side of the family...primarily in females. I'm a male, so what are my chances?

(I don't know anything about genetics, the last time I learned was in 8th grade when we learned some Mendelian genetics. Since then we've been learning Physics in science.)

 

Thanks,

antimatter

Posted

The thing is that we don't understand the causes very well. There are various treatments that can attack the plaque buildups in the brain, but we don't know if the plaque buildups are a cause or a symptom of something else.

 

Whereas with HIV we understand the virus and have no good way to fight it, with Alzheimer's we have an incomplete understanding and possible ways to fight it. It's a matter of time, really.

Posted
I'm not entirely sure what the plaque buildups are.

How do they affect the brain? What exactly are they?

There is a great article on Autophagy in the May 2008 Scientific American. It suggests that many diseases, including Alzheimers, are a breakdown in the autophagy process that normally keeps cells clean of debris from unused proteins and other products.

 

I just started reading it last night and it immediately fascinated me. It could be a real breakthrough in cellular strategies in medicine.

Posted

Ah, okay, I'll see if I can get a copy. My local library has almost every issue of sci-am.

Autophagy? It seems like it's exactly what Alzheimer's is, from my limited reading.

Posted

The gist of what I've read so far is that autophagy (aw-TOF-a-jee) is the process cells use to keep the cytoplasm tidy, and when this process is delayed or becomes inefficient then debris clogs the cells and problems occur, depending on where the cells are located.

 

With Alzheimers, a pigment called ceroid builds up inside neurites and that, coupled with accumulation of lipofuscin during normal aging, causes swelling in the neurites and amyloid plaque forms outside the swollen area, leading to neuron damage.

 

The article hints that a properly functioning autoghagy system could prolong life by retarding the aging process. It sounds a lot like the "clean-as-you-go" philosophy I'm trying to adopt at my house, where you clean up in little bits throughout the day so you don't have to do a major clean on the weekends. ;)

Posted

Thanks for the explanation, that was very helpful.

I'll go to the library tomorrow and check out the article.

 

How exactly does the process break-down? As in; what causes it?

(Apologies, I really don't know much about biology, despite my goal of being a doctor someday)

Posted

I haven't finished the article yet, but from what I recall it's a matter of the rate of the process; too slow and the cells clog with detritus, too fast and the cell literally eats itself. I'm not sure they know quite yet what causes the rate to fluctuate or malfunction. I know they are looking into ways to enhance and inhibit the process to combat cancer, Alzheimer's, Parkinson's and Huntington's diseases.

 

One drug, rapamycin, is looking promising for Huntington's patients. They use it now to stop the rejection of transplants and they've noticed that it stimulates autophagy and may clear up the protein aggregates that Huntington's patients exhibit.

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