Sleep Disorders as Prologue to Disease: From the Archives

What a (incremental) difference seven years make. In 2009, when we wrote about Dana Alliance member David Holtzman’s work, the headline was “Could Sleep Disorders Contribute to Alzheimer’s?” This month, Scientific American describes the work he and colleagues at Washington University School of Medicine in St. Louis are doing using the headline “Why Sleep Disorders May Precede Parkinson’s and Alzheimer’s.” We’ve gone from “maybe take a look” to “what’s the mechanism” on evidence for a link between sleep troubles and risk for neurodegenerative disorders has come.

Scientific American’s Simon Makin calls the Holtzman lab’s 2009 discovery the “best evidence for a causal relationship” From our story:

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The Blitz is On

Earlier this month, the senior vice president of the National Football League’s health and safety policy spoke at a hearing in Washington, D.C., where he was asked if there is a link between football and chronic traumatic encephalopathy, or CTE. Jeff Miller replied, “The answer to that is certainly, yes,” moving the ball down the field in a longtime debate among independent researchers, former athletes, and the NFL.

McKee_2012

Ann McKee, M.D.

Alongside Miller stood Dana Alliance member Ann McKee, M.D., whose latest study was just referenced in a story on CTE in the New York Times on Sunday, March 27. At the hearing, McKee presented findings from her ongoing research on the relationships between traumatic brain injury, neurodegenerative disease, and contact sports. As director of the Brain Bank for Boston University’s Center for the Study of Traumatic Encephalopathy, she has been making headlines over the past several years for revealing that “deceased athletes, including at least 90 former NFL players, were found to have had [CTE].”

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The How of Tau

The debate over whether the tau protein’s corruption is a cause or effect of the Alzheimer’s disease process is now all but over. In fact, its corruption seems to be a driver of disease not only in Alzheimer’s, but in more than half a dozen other tau-linked maladies.

The Dana Foundation’s latest briefing paper, “The How of Tau,” looks at how tau dysfunction kills and how scientists are working to stop it.

Since the early 1990s, autopsy studies have found that the spread of tau NFTs [neurofibrillary tangles and threads] through memory-related brain areas tracks the progress of Alzheimer’s dementia—and does so better than the spread of Aβ [amyloid beta] plaques. About fifteen years ago scientists also linked a familial form of the dementia syndrome known as frontotemporal dementia with parkinsonism to a set of tau mutations—whose effects turned out to be very similar to what is seen in Alzheimer’s. “Some of the mutations impair the binding of tau to microtubules, while others cause tau to aggregate more readily,” says John Q. Trojanowski, [M.D., Ph.D., a Dana Alliance for Brain Initiatives member who co-directs the Center for Neurodegenerative Disease Research at the University of Pennsylvania.]

Throughout the 2000s, scientists found more and more evidence that tau dysfunction kills and Aβ doesn’t—or rather that Aβ contributes to Alzheimer’s only indirectly, by causing tau dysfunction. The more conclusive findings have come only in the past few years. In 2011, for example, researchers in the Harvard Medical School laboratory of Dennis Selkoe, M.D. (also a Dana Alliance member) reported that small aggregates (“oligomers”) of Aβ, isolated from Alzheimer’s brains, triggered the hyperphosphorylation of tau as well as Alzheimer’s-like changes in neurons, including the loss of synapses, even at very low concentrations. This toxic effect was tau-dependent: no tau, no toxicity.

Read the full paper here.

–Ann L. Whitman

Cancer, Alzheimer’s may protect against each other

Diagnoses of Alzheimer’s
or cancer are never good news, but they may come with a small silver lining.

Scientists have found that having Alzheimer’s reduces the
risk for cancer, just as a diagnosis of cancer brings a reduced likelihood of developing
the brain disorder.

In a study
published online in Neurology

Dec. 23, scientists report on results from more than 3,000 people, all at least
65 years old, enrolled in an extended survey of cardiovascular health. Those
who entered the survey with Alzheimer’s had a 69 percent reduced chance to be
hospitalized due to cancer. Those who had cancer at the outset were 43 percent
less likely to develop Alzheimer’s, at least in Caucasians. (In other ethnic
groups, the opposite seemed to hold true, although sample sizes were too small
to provide reliable data in these populations.)

But no association was found between cancer and vascular
dementia, the second most common form of dementia after
Alzheimer’s. Unlike Alzheimer’s, which is characterized by abnormal proteins
that lead to brain cell death, vascular dementia stems from clogged blood
vessels that starve neurons of oxygen.

The reasons for these trends are not clear, since the study
looked at overall health trends and was not designed to investigate causes. But
the authors speculate that the findings imply that cancer and Alzheimer’s share
some common molecular basis that vascular dementia does not.

Previous studies have also found links between cancer risks
and neurological disorders. Parkinson’s
patients, in particular, have a
reduced risk for many cancers
; one possible cause, scientists think, is
that Parkinson’s causes increased apoptosis—or programmed cell
“suicide”—throughout the body, stifling many cancers before they have a chance
to establish themselves.

-Aalok Mehta

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