Antidepressants, Alzheimer’s and Brain Injuries: making bad worse


What we knew:lights-1088141__340

  • Use of antidepressants with Alzheimer’s patients increases the risk for falls and hip fractures
  • There is a protein found in the brain cells of persons with dementia and brain injuries that causes the Axon in the cell (electronic message transmitter) to swell and shut down. This protein is absent from normal cells. Elimination of the protein can cause the axon to start functioning again. (References are in previous blog.)

What the University of Eastern Finland has added to what we know:

  • Use of antidepressants with Alzheimer’s patients results in an increased incidence of traumatic brain injuries among these patients

The mechanism for the injury is probably falling. With slower mental processing and thus slower reflexes, these patients are less able to protect themselves when falling. That means a higher rate of concussions.

This ties back to another previous post on this blog — “deprescribing”. Drugs may have a value in one stage of a person’s life and be counterproductive at another stage. Doctors know how to prescribe drugs, but there are few protocols (apart for drug interactions) regarding when to stop taking a drug.  There is a group in Canada developing guidelines for deprescription, and while NIH has published articles on the topic, I’m not aware of any similar projects to develop guidelines in the US. Some US physicians appear to be doing this on an ad hoc basis.

I suspect deprescription is not a popular topic among pharmaceutical executives, but it needs to be addressed. Continuation of unnecessary medication is just one of many factors that bloats medical costs in the US — and why spending level no longer indicates quality of care. Unnecessary medication poses risks to some patients.


  1. Heidi Taipale, Marjaana Koponen, Antti Tanskanen, Piia Lavikainen, Reijo Sund, Jari Tiihonen, Sirpa Hartikainen, Anna-Maija Tolppanen. Risk of head and traumatic brain injuries associated with antidepressant use among community-dwelling persons with Alzheimer’s disease: a nationwide matched cohort study. Alzheimer’s Research & Therapy, 2017; 9 (1) DOI: 10.1186/s13195-017-0285-3
  2. University of Eastern Finland. “Antidepressant use increases risk of head injuries among persons with Alzheimer’s disease.” ScienceDaily. ScienceDaily, 9 August 2017. <>.
  3. Gurusamy Sivagnanam, “Deprescription: The prescription metabolism,”
    J Pharmacol Pharmacother. 2016 Jul-Sep; 7(3): 133–137.
    doi:  10.4103/0976-500X.189680
  6. Joaquín Hortal Carmon, IvánAguilar Cruz, FranciscoParrilla Ruiz, “A prudent deprescription model,” Science Direct, Medicina Clínica, Volume 144, Issue 8, 20 April 2015, Pages 362-369.


Restoring Brain Function


I don’t usually write about early or animal-phase research, but this is potentially quite important for those dealing with dementia, related illnesses, and brain injury.

The protein amyloid beta is believed to be the major cause of Alzheimer’s disease. This protein basically clogs cells and causes neurotransmitters in cells to become hyperactive, generating noise that interferes with thinking and memory.

That leaves three interesting questions:

  • What triggers the production of this protein?
  • Is there a way to shut production of the protein down?
  • What happens if we do?

A team of researchers at the University of Munich (Germany) have identified one such substance, of a category known as BACE inhibitors, that is effective in reducing the amount of amyloid beta in brain cells. Tested in mice, with the inhibitor included in their food for eight weeks, the result when beyond what the researchers expected:

As expected, the mice had less amyloid beta in their brain after this period, since its production was inhibited. However, the effect of the substance was much more far-reaching: the animals’ brain functions actually normalized. There were fewer hyperactive nerve cells, and the slow-wave brain patterns once again resembled those in healthy mice. A key finding for the scientists was the observation that the animals’ memory also improved.
(1 is the original journal article; 2 is the report in Science Daily for non-technical readers.)

Basically, functioning was restored to a level comparable to healthy animals who had never had the disease.

These researchers are planning a human clinical trial.

What makes this a really big deal is that amyloid beta is also a factor in traumatic brain injury (TBI). This presents a possible and quick route to restoration of brain function for both dementia and TBI victims. It is not a “cure” for either, but for the victim and their family, the potential is life-changing.

It’s amazing what you can find buried in a list of breaking scientific news.


  1. A. D. Keskin, M. Kekuš, H. Adelsberger, U. Neumann, D. R. Shimshek, B. Song, B. Zott, T. Peng, H. Förstl, M. Staufenbiel, I. Nelken, B. Sakmann, A. Konnerth, and M. A. Busche. BACE inhibition-dependent repair of Alzheimer’s pathophysiology. Proceedings of the National Academy of Sciences, 2017 DOI: 10.1073/pnas.1708106114
  2. Technical University of Munich (TUM). “Dementia: BACE inhibitor improves brain function: BACE inhibitor successfully tested in Alzheimer’s animal model.” ScienceDaily. ScienceDaily, 28 July 2017. <>
  3. . Amyloid imaging with carbon 11-labeled Pittsburgh compound B for traumatic brain injury. JAMA Neurol. 2014 Jan;71(1):23-31. PubMed.
  4. ALZFORUM, “Imaging Reveals Amyloid Up To a Year After Traumatic Brain Injury,” 16 November 2013.
  5. VE Johnson et. al., “Traumatic brain injury and amyloid-β pathology: a link to Alzheimer’s disease?” Nat Rev Neurosci. 2010 May;11(5):361-70. doi: 10.1038/nrn2808.
  6. Rebekah C. Mannix and Michael J. Whalen, “Traumatic Brain Injury, Microglia, and Beta Amyloid,” International Journal of Alzheimer’s Disease, Volume 2012 (2012), Article ID 608732, 5 pages.

Brain Injury and Football — No Place to Run


The latest evidence is pretty hard to ignore.

The research leader is Dr. Ann McKee, chief of neuropathology at the VA Boston Healthcare System and director of the CTE Center at Boston University. She examined the brains of 111 deceased NFL players. Of these, 110 had CTE, the degenerative disease caused by repeated blows to the head.

The marker for CTE is a protein found in damaged cells. Because it involves microscopic examination of brain cells, it can only be done after death.

However, families often don’t need that proof. While the victim is alive, they deal with issues such as early on-set dementia and suicide attempts.

The argument in the current report is that even if no one else in the NFL had CTE, the 110 proven cases would prove a statistically higher incidence of CTE among NFL players than in the general population. The bodies examined were a non-random sample of NFL players; families donated them because of concerns. However, the sheer number of cases makes the results statistically meaningful. There simply aren’t millions of NFL players.

And it seems likely that other players do have it. The skulls examined come from all playing positions on the American football field:

  • Linemen
  • Running backs
  • Defensive backs
  • Linebackers
  • Quaterbacks
  • Wide receivers
  • Tight ends
  • Place kickers
  • Punters

Everyone who plays is at risk.

More generally everyone is at risk. The major causes of brain injuries are car accidents and slip-and-falls. The difference between civilians and sports players is repetition. People don’t collect (hopefully) 5 or 10 concussions driving, but then can in football, soccer, auto racing, bike racing and other activities.

Even a single concussion can be devastating.

Like the cigarette debate of the 1970s, it’s time for fans and owners to move from denial to action. What do we do to care for the injured? Deal with suicide risks? Cover the costs of dementia c are?

There’s also the ethical question of whether people have the right to do things that will shorten their life. There is still an active debate on the ethics of assisted suicide in the US; doesn’t this fall into that discussion? If you opt to do something that you know can kill you, does it matter what the method is?


  1. “110 NFL Brains,” The New York Times, 25 July 2017.
  2. Gil D. Rabinovici, MD, “Advances and Gaps in Understanding Chronic Traumatic Encephalopathy,” JAMA, 25 July 2017.

Brain Injury: New Developments


imagesA brain protein, tau, may be an indicator of the length of time required for recovery from a concussion.

A research team from the National Institutes of Health and the University of Rochester Medical Center conducted a study of college athletes (NCAA Div. I and III) from a mix of sports.  Tau levels were measured preseason and within six hours following a concussion.

Tau was already a suspect in brain illnesses, having been identified as a factor in the development of chronic traumatic encephalopathy or CTE, frontotemporal dementia and Alzheimer’s disease.

Tau levels jump after concussion, and higher levels are linked statistically to longer recovery time requirements.

The research focused strictly on athletes and on defining an objective measure of when a player should be allowed to go back into play.  The report calls for follow-on studies including the capture of blood samples on the sidelines of games to assess how quickly tau levels change and whether that could be used as an immediate indicator.

However there are potential applications of tau to other situations and occupations, for example, people involved in traffic accidents and in law enforcement.  Is tau a potential measure of long term injury?  Could the metric be used to assess how long a worker should be out after a work-related injury?  Frankly, if tau works for athletes, it’s hard to see why it wouldn‘t work in these other situations.


  • Jessica Gill, Kian Merchant-Borna, Andreas Jeromin, Whitney Livingston, Jeffrey Bazarian. Acute plasma tau relates to prolonged return to play after concussion. Neurology, 2017; 10.1212/WNL.0000000000003587 DOI: 10.1212/WNL.0000000000003587
  • University of Rochester Medical Center. “Brain protein predicts recovery time following concussion.” ScienceDaily. ScienceDaily, 6 January 2017. <>.


New Tools for Seeing Brain Injuries


snyder-the-unseen-victims-of-traumatic-brain-injury-from-domestic-violence-1200One of the limitations on doctors ability to treat many diseases is the inability to see the disease.  That’s true with many cancers, where the exact boundaries of a cancer aren’t visible and isolated cell clusters can be missed entirely.  It’s especially true with brain injuries, where relatively subtle dislocations of neurons can have massive consequences on functioning, pain and quality of life.

It’s also been a complaint of trial lawyers in injury cases.  Juries can see wheelchairs and crutches.  Internal injuries, especially of the brain, often don’t exhibit outward signs and make it harder to prove injury to skeptical panels.

Now, researchers at a Canadian university (Simon Frasier University in British Columbia) have developed a new use for a high resolution brain scan technology in the identification of brain injuries.  This technique reportedly can identify injuries that are invisible to traditional CAT scans and MRIs cannot.

The technology is magnetoencephalography, or MEG. The method was pioneered at the University of Illinois in 1968 by physicist, David Cohen.  It’s use to date has been to understand and map brain activity and assess seizures in epilepsy. The strength of MEG is precision: it measures brain activity in much smaller time increments and measures electronic signals that are quite faint relative to the environment in which most people function.

The use  use of MEG to assess brain injury is new.  This approach maps the passing of electronic signals between different regions of the brain.  Changes in these patterns can identify injury when actual damage is too subtle to detect.  Statistical modeling allows the doctor to determine the location of injury.

Why does  this matter?  We’ve seen how brain injuries can affect quality of life and even the ability to follow commands and make critical decisions in crisis situations.  We’ve also heard testimony from people who have been injured and been accused of “faking it.”  Now we may have the ability to prove injury in the absence of outward physical signs and make better decisions about what to do with people with real hurt.

MEG, like other leading technologies, is not readily accessible to people in all parts of the US.  That makes the case for supplement insurance (e.g., the Aflac Accident Policy) to pay for travel that may be required for state-of-the-art treatment.



Brain Injuries and Domestic Violence


A new study finds that traumatic brain injury (TBI) is a common result of domestic violence.  This in turn may affect how victims behave and the medical treatment they snyder-the-unseen-victims-of-traumatic-brain-injury-from-domestic-violence-1200require.  It should affect how police and EMTs approach domestic violence situations.

According to Dr. Glynnis Zieman, the lead researcher at St. Joseph’s Hospital and Medical Center in Phoenix:

“Head injuries are among the most common type suffered in domestic violence, which can lead to repetitive brain injuries that often have chronic, life-changing effects, much like what we see in athletes. We found that 88 percent of these victims suffered more than one head injury as a result of their abuse and 81 percent reported too many injuries to count.”

The Barrow Neurological Institute at St. Joseph’s has established a specialized program to treat TBI resulting from domestic violence.  This program is believed to be the first of its kind in the US.

Why does this matter?

Among other things, women who are battered are often unwilling to leave abusive partners.  Brain injury resulting in an inability to think and act rationally could explain much of that behavior.  The lag between abuse and leaving a situation may be less due to emotional stress than due to the need to recover at least in part from a serious injury.

Women who are battered need to be evaluated for brain injury.  That may mean hospitalization away from the abuser, as well as treatment and counseling for TBI.  If TBI is involved, it can have long term consequences for the victim, and the penalties for the abuser should be much  more severe.

“The medical team has found many victims are suffering from a full spectrum of side effects that can lead to the loss of a job, income, and eventually homelessness.”

The victims of abuse simply don’t have the financial resources available to celebrity athletes, but may face the same consequences in terms of cognitive decline, decline in motor skills and early death.

The New Yorker ran a remarkable story on brain injury and domestic violence in December 2015, well before this research was available.(4)  While that was anecdotal evidence of a problem, now we have an understanding of just how widespread this problem is.

This is a big deal.

The next logical question is, what about battered children?



  1. Glynnis Zieman, Ashley Bridwell, Javier F. Cárdenas. Traumatic Brain Injury in Domestic Violence Victims: A Retrospective Study at the Barrow Neurological Institute. Journal of Neurotrauma, 2016; DOI: 10.1089/neu.2016.4579
  4. Snyder, Rachel, “No Visible Bruises: Domestic Violence and Traumatic Brain Injury,” The New Yorker, 30 December 2015.

Some Dreams . . .


I love this poem, written by Lyn.

Tumbling © Lyn Crain


Here I am,

the hero of my empire

in this long shadow

of being mortal.

I contain multitudes

in this pigeon tunnel

that I once believed was

an ivory tower

before my downfall.

The power of I am,

me before you. I became

a stranger in my own mind

absurd and realistic.

Maybe or maybe not,

a timeless observer or

an unhinged loner,

a train wreck for sure

after you!

A great reckoning with

the best of words

my breath became air,

apprenticed in death.

I let you go

my runaway dream.