Brain research enters 'golden era' at Stanford | January 6, 2017 | Palo Alto Weekly | Palo Alto Online |

Palo Alto Weekly

- January 6, 2017

Brain research enters 'golden era' at Stanford

Alzheimer's center accelerates new studies, trials, drugs

by Chris Kenrick

For patients suffering from Alzheimer's disease, little progress in the way of treatment has been made for decades, says Stanford neurologist and biotechnology pioneer Frank Longo, who chairs the Department of Neurology and Neurological Sciences, co-leads the new Stanford Neuroscience Health Center and serves as associate director of the Stanford Alzheimer's Research Center.

"When I walk into our Memory Disorders Clinic, it's very embarrassing for me that I cannot offer any drug better than what we had 20 years ago," he recently told those gathered to hear him speak at Palo Alto's Avenidas senior center. "We have nothing to delay onset or slow progression, and it kills me every time when I see my families, my patients, and I can't offer anything better."

Longo is determined to change that. He, along with dozens of Stanford researchers from multiple disciplines, have been working with the Stanford Alzheimer's Research Center to conduct interdisciplinary research on the disease and related disorders since 2015 when the National Institute of Health provided $7.3 million to open the center and support five years of research. The center is one of more than 30 institutions funded as a federal Alzheimer's Disease Research Center.

"We've entered the golden era for neuroscience, I think," said Longo whose pioneering work earned him the inaugural 2015 Melvin R. Goodes Prize for Excellence in Alzheimer's Drug Discovery from the Alzheimer's Drug Discovery Foundation and landed his efforts on the cover of Time Magazine last February.

He said the center has given researchers the ability to accelerate their studies by enabling them to gather data — brain scans, blood tests, spinal taps — from a group of subjects and create a body of data that the faculty can tap into with their ideas about better ways of diagnosing and treating the disease, which is among the most common neurodegenerative disorders in the nation. Alzheimer's affects about 5.1 million Americans. By 2050, that number is expected to increase to 13.8 million, according to statistics from Stanford University..

"(Researchers at the clinic) have all this information that they can't get from a mouse," Longo added."This is the fuel that will change this situation and give us something better to offer than we offered 20 years ago."

Those working with the center already have a range of research in the pipeline as well as a new push to recruit subjects to study what happens inside the brain during Alzheimer's earliest stages.

For the first time this month, Longo began clinical testing of an oral drug on Alzheimer's patients that he, his team and collaborator Dr. Stephen Massa pioneered. When tested on mice, the experimental drug (referred to as C31) showed to keep nerve cells from degenerating by strengthening their protection against neurological attacks. If the trials prove successful, C31 could become the first treatment to prevent the disease rather than treat its symptoms.

Other research at the center has identified possible "protective genes" against the effects of brain degeneration.

"Right now," Longo said, "one of the biggest mysteries is: you can take two brains from patients; they have the same amounts of amyloid and tau (both are proteins in the brain that interfere with synaptic connections), and one person can barely function and the other is functioning normally. Why? There's something about the functioning person that their brain is able to resist that amyloid and tau. One idea is that it's because they've stayed active; another theory is that there's something in the brain that's protecting it."

Longo said the greatest barrier to getting effective therapies to people "is that it's so hard to know what's going on in the brain with Alzheimer's disease. If we understood that, we'd be developing therapies at tenfold the rate we are now, and they'd have a greater chance of being effective."

As part of the push to better understand the onset of the disease, Stanford's Alzheimer's Center is currently seeking research subjects in various categories, including healthy volunteers as well as people in the early stages of Alzheimer's, Parkinson's, Lewy Body disease or mild cognitive impairment.

Volunteers are asked to come to Stanford for a neurological examination, cognitive tests and questionnaires, one or two MRI brain scans, a blood draw and, in most cases, a lumbar puncture to obtain spinal fluid. They are asked to return in a year for more evaluations and also to consider eventual brain donation.

Palo Alto resident Romola Georgia said she came upon a flier for Stanford's "Healthy Brain Aging Study" after participating in the October 2016 Walk to End Alzheimer's, and has signed herself up as a healthy volunteer.

Georgia, a cellist and gardener who also raises chickens in her yard, described the challenges of caring for her husband over the past six years as minor lapses in his early 70s have developed into advanced dementia.

"The path of dementia is confusing, challenging... and undermines everything you've come to assume about your family, your relationship and the future," Georgia said, adding that she is pleased to be able to help with the research.

While other federal Alzheimer's Disease Research Centers have focused on later stages of the disease, Stanford is particularly looking for people in the early stage of Alzheimer's or its precursor, mild cognitive impairment, said psychologist Dolores Gallagher Thompson, a research professor of psychiatry and behavioral science.

"Why it is that some people with mild cognitive impairment go on the develop Alzheimer's disease and some don't?," Gallagher Thompson said.

"That's the 64-million-dollar question. There are lots and lots of older people with symptoms that would qualify as mild cognitive impairment, but nobody knows what that means because we don't really know whether that's going to progress to Alzheimer's.

"So in our center we're trying to get as any people as possible with the 'mild cognitive impairment' label — either they already know they have it, or they come in and we test them and we tell them they have it."

Longo said the best research-tested precaution people can take to reduce their risk of Alzheimer's is to exercise 30 minutes a day for five days a week. He also recommends a Mediterranean diet as part of an overall plan to reduce risk of Alzheimer's, high blood pressure and diabetes. Still, there are no guarantees.

For more information, go to med.stanford.edu/adrc or contact Christina Wyss-Coray at ADRCstanford@stanford.edu.

Contributing writer Chris Kenrick can be emailed at ckenrick@paweekly.com.

Comments

Posted by Ugh!, a resident of Midtown
on Jan 6, 2017 at 2:21 pm

Ugh! is a registered user.

Stanford concentrates on research and more research, burning money all the while with conclusions that are,more often than not, utterly useful.

Meanwhile, UCSF concentrates on results and comes up with cures.

This may be a reason why Stanford Med School grads are less desirable as hospital residents and doctors than UCSF Med School grads.


Posted by john_alderman, a resident of Crescent Park
on Jan 6, 2017 at 8:33 pm

john_alderman is a registered user.

@ Ugh - That's fairly petty, isn't it? The article is largely about Dr. Frank M. Longo who in /collaboration/ with Dr. Stephen Massa at UCSF, discovered a new alzheimer's medication. Two schools, getting along, working together..


Posted by ohgosh, a resident of another community
on Jan 7, 2017 at 10:59 am

As a volunteer participant in this research, I am sorry that someone deems this endeavor at Stanford to be useless. Much is learned from these efforts --every discovery is not suddenly presented in a beautiful gift-wrapped package for those involved in the search. It is a long, arduous goal that comes with continued work and patience and the day will come when the findings will pinpoint the conclusions that are made toward the ability to quell the monsters that rob the mind in old age or before. How is anything worthwhile attained? I sense some sour grapes from one who might have tried to become a part of the Stanford Medical School but somehow did not made the grade. The researchers are all in this together regardless of where they are planted.


Posted by read it, a resident of Midtown
on Jan 7, 2017 at 6:23 pm

Hey Ugh!, "utterly useful" is a good thing.


Posted by anne, a resident of Green Acres
on Jan 8, 2017 at 7:06 am

"You can take two brains from patients; they have the same amounts of amyloid and tau (both are proteins in the brain that interfere with synaptic connections), and one person can barely function and the other is functioning normally. Why?"

The other question I would ask is, why have dementia rates in the US dropped 24%, which is huge - have other nations seen a similar improvement? Why are people with more education less prone to dementia? Are those facts related?

My grandfather developed dementia symptoms pretty late. My mother and aunt complained that he could barely speak and was forgetting everything. When I spoke with him, I couldn't tell what they were talking about, he seemed little different. The difference is that his daughters spoke with him in their native language, but I spoke with him in English and the language he had used in school, both of which he had spent most of his life learning and relearning, and probably worked different parts of his brain than his native tongue. It's sad that we diidn't compare notes until later, after my mom had realized my grandfather was much more normal if she spoke with him in English. Then she said it was as if he was forgetting his native tongue (less like he was forgetting everything completely).

At one point in my own life, undiagnosed infection robbed me of my ability to speak and read in the other language besides English that my grandfather and I shared (among much else). The assumption was that the language was simply lost because .i wasn't studying it, even though I was reading great literature in that language on a regular basis. When the disease was properly treated, I was surprised to fibd I was suddenly able to read in that language again. I have always thought the issue was the part of my brain able to access the language. The process that took away that ability was likely affecting my system and brain for some time before it hit that particular part.

Perhaps the dementia is related to where the brain is affected more than the fact that there are plaques (or other reasons for damage). Perhaps we all have different pathways to compensate, and educated people perhaps have more, and it isn't until they are all compromised that dementia becomes obvious. Since dementia is likely caused by many things, the ability to work with individuals to figure out how to restore each individual's cognitive function or to protect each person's cognitive health individually is pretty important. I don't see that happening yet, especially not as a major research approach.

Anyway, while I disagree with the idea that answers have to be slow and incremental @ohgosh, I certainly agree with you that longterm research is critically important and that this work described here at Stanford is a fresh approach. I would just hope to see a greater number of different approaches and better guidelines for empirical work with individuals, too.

I understand the concern of seeming to experiment on people, but given the facts pointing to so many differences, perhaps it's time we developed guidelines for ethical empirical work with individuals. Perhaps the evidence points to dementia being many things, and continuing to approach it from a population and single treatment perspective will never work well. Can we develop an armament of things that is worth just trying? For example, some researchers propose evidence of certain kinds of infections - developing better antibiotics to cross the blood brain barrier, with minimal side effects, would allow researchers to simply try something to see if it helps, who it helps, when it helps, even how it helps (in combination with other drugs? a slow treatment over time? etc)

Given that little has changed in 20 years for patients, it might be helpful to revisit Thomas Kuhn's Structure of a Scientific Revolution, the work from which the word "paradigm" became popularized. The hallmark of a paradigm on its last legs, in need of shifting, is that fewer and fewer problems are solved, making advances takes more and more time and manpower, and advances are incremental and slow. With a nod to the above, perhaps the answer may be in another part of the collective brain, and we must consider also taking radically different approaches, simultaneously, not just in Alzheimers work, but also in cancer, etc. The actual science is going through a revolution while treatment results continue to take mostly small steps, per results. How do we change that?


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