A call for more research on “chemobrain”

Image credit: Microsoft

The journal Trends in Neurosciences published an article June 12, 2018 calling for more research into cognitive impairment caused by cancer treatment.    Unfortunately, it’s behind a paywall.  To get an overview of the content,  read Cancer Today’s July 18, 2018 article “What is ‘Chemobrain’?” , which is an interview the article’s lead author, Todd Horowitz of the National Cancer Institute.


My Norwescon 39 Panel Schedule

nwc 2016 banner

The Norwescon 39 Science Fiction Convention happens March 24-27, 2016, in SeaTac, Washington.  I will once again be a science panelist.  You can find me on the panels listed below, or maybe hanging out in the bar with other writers and science geeks, scarfing down a snack in the Green Room, or wandering the corridors on my way to the art show, dealers room, a friend’s reading, or an interesting panel.  hope to see you there!


BIO21 – Blinded by Pseudoscience
Fri 6:00 PM-7:00 PM – Cascade 3&4
Gregory Gadow (M), Janet Freeman-Daily, Caroline Pate, Dr. Misty Marshall, Jake McKinzie

TEC05 – Real Radiation for Writers & Readers
Fri 8:00 PM-9:00 PM – Cascade 5&6
Mike Brennan (M), Janet Freeman-Daily, Arthur Bozlee, Daniel P. Lynge

BIO20 – Facts & Fictions of Cancer
Sat 1:00 PM-2:00 PM – Cascade 5&6
Janet Freeman-Daily (M), Dr. Misty Marshall, Vickie Bligh, Nicholas Maurice

BIO16 – Ask the Experts: Biology
Sat 2:00 PM-3:00 PM – Cascade 5&6
Alan Andrist (M), Janet Freeman-Daily, Caroline Pate, Dr. Misty Marshall, Nicholas Maurice

TEC01 – Remembering In Tomorrow
Sat 7:00 PM-8:00 PM – Cascade 9
Sean Hagle (M), Janet Freeman-Daily, Michael Ormes

BIO19 – Evolution Is Just a Theory!
Sun 10:00 AM-11:00 AM – Cascade 5&6
Dr. Ricky (M), Janet Freeman-Daily, Alan Andrist, Michael McSwiney, Jake McKinzie

BIO03 – Future Pharma
Sun 2:00 PM-3:00 PM – Cascade 5&6
Janet Freeman-Daily (M), Caroline Pate, Vickie Bligh, Nicholas Maurice

Building cognitive skills after chemobrain

Earlier this month the MIT News published an article titled, “The rise and fall of cognitive skills.”  It discussed research that found different types of thinking skills peak at different times in life.  I particularly like this part:

… crystallized intelligence — the accumulation of facts and knowledge … showed a later peak, in the late 60s or early 70s.

People who participated in this online study demonstrated their ability to build their vocabulary continued to increase into their 60s and 70s, which indicates their ability to accumulate facts and knowledge also continued to increase.  This is awesome!   As a person in my 50s with cognitive impairments from cancer treatment, I’m reassured to know that at least some parts of my brain may continue to improve.  Woohoo!

Now if I can just remember what I learn …



Neuropsych Serendipity

I visited the Virginia Mason Neuropsychology and Rehabilitation department today for a consult about dealing with my chemobrain symptoms.

I expected the appointment to be an introductory session: the counselor and I would spend the time recounting my cancer history, detailing my symptoms, explaining the chemobrain study in which I participated at Fred Hutchinson Cancer Research Center last year, learning about therapy options, and discussing possible neurocognitive testing.

Turns out the Ph.D. psychologist I saw was the lead researcher for last year’s chemobrain study!

She knew me.  She knew my history. She had access to my previous neurocognitive results from the trial.  The available therapy options were the techniques she and her team had taught me last year.

So, we spent a VERY productive hour talking about coping strategies for my particular symptoms and situations.

Might this be cosmic payback for volunteering for clinical studies?

Serendipity rocks.


brain 2 graphic


Last Monday and Tuesday, September 8-9, I was in Denver for my clinical trial at University of Colorado Hospital (UCH). I had my once-every-eight-weeks PET-CT scan along with a once-every-six-months brain MRI.

I’m happy to report that both scans were clean. I’m now twenty months with No Evidence of Disease of metastatic lung cancer.  That Xalkori is great stuff for those of us with ROS1 NSCLC!

I’ve been in my clinical trial for 22 months, and the trial has been running for over three years. The medical journal article summarizing trial results is due out sometime in the next two weeks.  Judging from the response to Xalkori of several ROS1ers I’ve met online, I expect the news will be positive.  Can’t wait to read it–I’ll probably hustle to the University of Washington Library and download it first chance I get.  Yes, besides being a science geek, I’m an INTENSE science geek.  One of those “complete response” lines on the waterfall plot will be ME!

The scanxiety for this visit was different than my previous visits to Denver. It’s been a very busy summer for me.  As I posted previously, before flying to Denver I attended the Stanford Medicine X conference in Palo Alto September 4-7.  I gave my speech on lung cancer stigma on the main stage Sunday morning, left the conference a couple of hours early to fly to Denver Sunday night, and had my clinical trial labs and scans Monday.  I was so focused on the conference and my speech that I barely noticed any scanxiety –it was difficult to distinguish from the intensity that precedes my speaking publicly.  The only real indication of any anxiety was my increasing inability to focus during the conference and three hours of lost sleep the first night in Palo Alto (although my husband might have a different perspective about my intensity in the days before I flew to Palo Alto).

A few other things were different about this clinic visit:

  • On the day of my visit, I spent an hour talking with the American Lung Association of Colorado’s office about LUNG FORCE.
  • A pleasant UCH oncology Fellow conducted my clinic visit. My primary oncologist Dr. Camidge came in to chat with us both for a few minutes afterwards–he knows I always have a list of questions for him. We talked about an exciting new clinical trial design at UCH for FGFR-positive NSCLC (more on that in a future post).
  • UCH had recently installed new software for their MRI machine, so the report of my brain MRI was not available at the time of my clinic visit. However, Dr. Camidge and the Fellow both reviewed the scan itself and reassured me it was normal.
  • After Dr. Camidge completed his clinic hours on Tuesday, he joined me, Dora (an online friend of mine who is also his lung cancer patient), and Dora’s husband Bill for a chat at a restaurant near UCH. How many world-renown lung cancer doctors do that? Well, yes, I did bribe him with a cup of coffee and a pastry. Here’s a selfie we took:

selfie with Camidge

Something else was also new to me after this clinic visit. I had a headache after I arrived home.  Since I’d just had a clean brain scan two days before, I knew the cause could not possibly be a brain met.  Somehow this reinforced the feeling that I was more a normal person than a cancer patient at this point.  Sometimes a headache is just a headache.

The brain MRI report appeared in our mail yesterday. It didn’t say much except “normal,” but a few terms were new to me.  I was Googling the new terms when an infolinks box popped up with this message:

“Searching for T2 hyperintensities in white matter? Try Kelley Blue Book!”

Maybe Kelley Blue Book can tell me how my hyperintensities affect the resale value of my brain.

Finding Good Biomedical Science Articles

Every day patients with cancer and other health issue turn to the Internet to learn about symptoms, causes, and treatments for their conditions. Consumers have many good options for consulting “Dr. Google.” Some websites (like mayoclinic.com) have outstanding credentials for providing medical information. Other sites like PubMed are good places to search for biomedical journal articles.

But not all online biomedical journal articles contain good science.

Science magazine–a premier, peer-reviewed science journal–recently conducted an experiment in which a correspondent submitted a biomedical research paper to open access journals for publication. Open access journals rely on author fees rather than subscriptions. The paper announced a new treatment for cancer derived from lichens. Its science and conclusions were clearly flawed, which should have been caught by each journal’s peer review process. Yet many of the journals published the flawed paper anyway.

This is why I stick to PubMed and journals of demonstrated quality as sources for biomedical articles. It isn’t a foolproof method for finding good science, but it’s better than just googling a topic. You simply can’t believe every headline or abstract you read.

Diabetes Slows the Progress of Alzheimer’s

People with diabetes are known to be at higher risk for developing Alzheimer’s disease.  However, the interaction between the two diseases is not well understood.  A French study published 10/27/2009 just found that Alzheimer’s progresses more slowly in people who have diabetes.   An article on DiabetesHealth.com says:

“Diabetes is thought to increase the risk of developing Alzheimer’s, possibly because of vascular damage in the brain that mimics the dementia seen with Alzheimer’s.  But once patients display symptoms of the disease, the current study suggests that the progression is slower than in people without diabetes. … One complication may be that the medications used to help control blood sugar have a protective effect on the brain….”


Jumping with Glial

Most of us have heard of neurons.  But have you ever heard of glial cells?   They make up almost 90% of the brain, and science is beginning to explore what they do and how they might contribute to thought.  Originally thought to simply be the “brick and mortar” that insulated neurons,  glial cells are now known to communicate with each other and with neurons,.  They can produce neurotransmitters, and they appear to be essential for forming new neurons and connections between neurons.  Who knew?

Scientific American interviewed Andrew Koob (Ph.D. is neuroscience from Purdue University) about glial cells and why they orginally got no respect.


Concussions can lead to dementia

The “60 Minutes” TV program recently ran a segment on long-term effects of concussions sustained in sports.  First associated with pro boxers, chronic traumatic encephalopathy (CTE) is a condition seen only in people who suffer repeated dazing blows to the head.  It is  diagnosed after death by examining brain tissue for abnormal proteins that show up as dark brown pigment in brain sections.  These proteins are neurofibrillary tangles of tau, which are also characteristic of Alzheimer’s and other dementing illnesses.  CTE has been diagnosed in the brains of several deceased pro football players over the past few years.

Dr. Ann McKee, a neuropathologist at Boston University School of Medicine, has been working on a brand new area of research on the brain that has provided physiological proof of brain disease in athletes who have suffered concussions.  …

“I’ve looked at brains from people that have lived to be 110. And you just don’t see anything like this, what we see in these athletes,” she told Simon

Even more troubling, she says, CTE actually progresses undetected for years, silently eating away at brain cells, until it causes dementia and other cognitive problems.

“It seems to be triggered by trauma that occurs in a person’s youth; their teens, their 20s, even their 30s. But it doesn’t show up for decades later,” she explained. “People think it’s a psychological disease or maybe an adjustment reaction, maybe a mid-life sort of crisis type of thing. But actually, they have structural disease. They have brain disease.”

Dr. McKee’s research found that athletes in any contact sport are at risk of permanent brain damage.

You can see the video and read more at  http://www.cbsnews.com/stories/2009/10/08/60minutes/main5371686.shtml

In retrospect, I sure am glad dear old Dad (a general practioner) forbade me from playing contact sports while growing up!

Detecting Alzheimer’s Before Symptoms Appear: ADNI

The Alzheimer’s Disease Neuroimaging Initiative (ADNI) (http://www.adni-info.org/) aims “to study the rate of change of cognition, function, brain structure and function, and biomarkers” over 5 years, starting in October 2004.  Its 800+ participants–which include healthy elderly controls, subjects with mild cognitive impairment (MCI), and those with Alzheimer’s disease (AD)–undergo magnetic resonance imaging (MRI) and positron emission tomography(PET) scans along with laboratory (blood, urine, and cerebrospinal fluid, or CSF) and cognitive tests.   One unique aspect of this huge study is that data from the 58 research sites is posted online and made available free to qualified researchers.  This is the largest public-private brain research project ever funded by the National Institutes of Health.  It has spawned similar efforts in Europe, Australia, Japan, and elsewhere.

ADNI searches for biomarkers that can determine AD risk.  Blood pressure is a biomarker that helps determine risk for heart disease or stroke.  Among other things, ADNI seeks to find a combination of biomarkers that are a clear indicator of AD.

The initial ADNI goal was to create a standard assessment tool for use in AD clinical trials.   Current methods for assessing the progress of AD in patients are slow and not always reproducible.  Clear, precise measures of the disease process would make it easier to determine whether someone is improving or declining on a new treatment.  Also, if all trials were using the same measures of success, it would be easier to compare results of different treatments.  This would make clinical trials less costly and produce reliable results more quickly.

The study is flexible enough to incorporate new technologies.  After the study began, the ability to detect amyloid beta in the brain in living subjects using PET was demonstrated.   This was the first time the characteristic accumulation of the protein in the brain could be confirmed without benefit of autopsy. This measurement was added to the study at some sites.

As ADNI research progressed and scientists became aware of new ways its data could be applied, the study’s goals expanded.  Over 800 blood samples underwent whole genome analysis as part of the search for AD-associated genes.  The ADNI samples have the benefit of donor brain scans and lab data available to researchers.  Analysis has identified several new genes (in addition to the 4 known early onset AD and 1 late onset AD genes) as targets of study, and researchers are working to confirm they are associated with increased risk of AD.  http://homepages.indiana.edu/web/page/normal/10543.html

Near the end of the study, ADNI is yielding fascinating results.  Detecting the beginnings of AD, before the onset of symptoms, might allow treatments that postpone onset of symptoms and maybe someday even prevent symptoms from occurring.  It’s long been known that amyloid beta and tau proteins accumulate in the brains of AD victims.  Tools like MRIs and CSF tests may reliably detect AD before symptoms appear and predict whether MCI will convert to AD.   One ADNI result shows when people develop AD, the concentration of amyloid beta 42 in CSF drops and tau increases.  http://www.medicinenet.com/script/main/art.asp?articlekey=92513

ADNI ends in October 2009, with final results reported in 2010.  To date over 25 papers have been published with many more under review and presented at conferences.  Proposals are in work for ADNI 2.