Cover Image: January 2010 Scientific American Magazine See Inside

Immune Response May Worsen Alzheimer's

The body's immune response may speed up memory loss in Alzheimer's














Share on Tumblr

Inflammation in the body has gotten a bad rap recently, thanks to the exacerbating role it may play in health problems such as heart disease and cancer. Now there may be one more malady to add to the list: Alzheimer’s disease.

When inflammation arises in the body as a result of infection or injury, the immune response also appears to accelerate memory loss in people with Alzheimer’s, according to a recent study published in the journal Neurology. In this study of changes in patients’ cognitive abilities over a span of six months, Alzheimer’s patients who had chronic (ongoing) inflammation as a result of, for instance, obesity or arthritis experienced four times the amount of memory loss as compared with patients without such inflammation. And those with chronic inflammation who also experienced an acute immune response (short-term, such as from an infection) were even worse off: their memory loss accelerated 10 times faster than patients without any inflammation.

“When we started the study, we thought short-lived events would be impor­tant,” says lead author Clive Holmes, a professor of biological psychiatry at the University of Southampton in England. “We hadn’t realized how important chronic inflammation was going to be.”

So how does inflammation, whether from an infection or from chronic dis­ease, damage the brain? The answer lies in the body’s immune response, which launches an attack on invading pathogens, releasing inflaming proteins such as tumor necrosis factor, or TNF. This molecule causes the vagus nerve, which extends from the brain to the abdomen and controls vital functions such as heartbeat, to send an electrical im­pulse to the brain, thereby directing the brain to secrete its own immune messengers.

In people with healthy brains, this chain of events merely leads us to feel under the weather for a few days. But cells in the brains of Alzheimer’s patients may be in a constant state of low-level inflammation. Therefore, if they are exposed to a pathogenic threat or chronic disease, they can leap into full-fledged inflammation, releasing compounds that ultimately kill brain cells. Scientists aren’t quite sure why cells end up dying, but some neurons may be annihilated in an effort to stop the virus’s spread, whereas others could be destroyed by accident in the quest to rid the body of invaders, Holmes says.

The study’s results could help physicians minimize Alzheimer’s memory loss by cutting chronic inflammation, such as by helping their patients lose excess weight. Or researchers could try to aim right at the source: “If inflammation in the body is causing [inflammation] in the brain and if you can dampen that signal, blocking TNF could play a role in slowing Alzheimer’s disease,” Holmes states.

Note: This story was originally printed with the title "Inflamed Neurons"


Buy This Issue
If your institution has site license access, enter here.

Comments

Add Comment
Leave this field empty

Add a Comment

You must sign in or register as a ScientificAmerican.com member to submit a comment.
Click one of the buttons below to register using an existing Social Account.

More from Scientific American

Follow Us:

See what we're tweeting about

Scientific American MIND

More »

Free Newsletters


Get the best from Scientific American in your inbox

Solve Innovation Challenges

Powered By: Innocentive

  SA Digital
  SA Digital

Science Jobs of the Week

Email this Article

Immune Response May Worsen Alzheimer's: Scientific American Mind

X
Scientific American Mind

Subscribe Today

Save 66% off the cover price and get a free gift!

Learn More >>

X

Please Log In

Forgot: Password

X

Account Linking

Welcome, . Do you have an existing ScientificAmerican.com account?

Yes, please link my existing account with for quick, secure access.



Forgot Password?

No, I would like to create a new account with my profile information.

Create Account
X

Report Abuse

Are you sure?

X

Institutional Access

It has been identified that the institution you are trying to access this article from has institutional site license access to Scientific American on nature.com. To access this article in its entirety through site license access, click below.

Site license access
X

Error

X

Share this Article

X