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

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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.


Sources:

  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. <www.sciencedaily.com/releases/2017/08/170809073627.htm>.
  3. Gurusamy Sivagnanam, “Deprescription: The prescription metabolism,”
    J Pharmacol Pharmacother. 2016 Jul-Sep; 7(3): 133–137.
    doi:  10.4103/0976-500X.189680
  4. http://deprescribing.org/
  5. http://www.drjohnm.org/2014/10/to-deprescribe-adding-a-new-verb-to-the-language-of-doctoring/
  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

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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.


Sources:

  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. <www.sciencedaily.com/releases/2017/07/170728100937.htm>
  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. http://www.alzforum.org/news/research-news/imaging-reveals-amyloid-year-after-traumatic-brain-injury
  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. http://dx.doi.org/10.1155/2012/608732

Dying at Home

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Alzheimer’s if the primary cause of dementia in the US. It current impacts 5.5 million

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Incidence of Alzheimer’s by county in US

American adults, and that number is expected to increase to 13.8 million by mid-century.

What’s important is the shift in Alzheimer deaths from medical facilities to the home.

  • In 1999, 67.5% of Alzheimer’s deaths occurred in a nursing home or long term care facility; by 2014, that figure had fallen to 54.1%
  • In 1999, 14.7% of Alzheimer’s  deaths were in a hospital; in 2014, that had fallen to 6.6%.
  • In 1999, 13.9% of these deaths occurred at home; by 2014, this number had risen to 24.9%.
  • In 2014, 6.1% of the deaths were in hospice care.

What we can’t tell from these data are whether families are bringing loved ones home right before end of life, or whether they simply can’t afford the high cost of long term care facilities.

The data also don’t tell us the extent to which families are now relying on home health care services in lieu of nursing homes.


Sources: Taylor CA, Greenlund SF, McGuire LC, Lu H, Croft JB. Deaths from Alzheimer’s Disease — United States, 1999–2014. MMWR Morb Mortal Wkly Rep 2017;66:521–526. DOI: http://dx.doi.org/10.15585/mmwr.mm6620a1

 

Alzheimer’s — latest news

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This is in an early stage of testing, but is worth knowing.  A Greek research team is experimenting with a virtual reality game that can be used as a self diagnostic tool for detecting early stage mild cognitive impairment (MCI).  MCI is a precursor to Alzheimer’s. Early detection of MCI can allow medical treatment that can either delay or prevent the development of Alzheimer’s.

“MCI patients suffer from cognitive problems and often encounter difficulties in performing complex activities such as financial planning. They are at a high risk for progressing to dementia however early detection of MCI and suitable interventions can stabilize the patients’ condition and prevent further decline.”

The the virtual supermarket remote assessment routine is able to classify individuals with MCI 91.8% of the time, on a par with diagnostic tests administered by professionals.

And that, people, is a remarkable step in dealing with one of the most horrific diseases among humans today.


Sources:

  1. Stelios Zygouris, Konstantinos Ntovas, Dimitrios Giakoumis, Konstantinos Votis, Stefanos Doumpoulakis, Sofia Segkouli, Charalampos Karagiannidis, Dimitrios Tzovaras, Magda Tsolaki. A Preliminary Study on the Feasibility of Using a Virtual Reality Cognitive Training Application for Remote Detection of Mild Cognitive Impairment. Journal of Alzheimer’s Disease, 2017; 56 (2): 619 DOI: 10.3233/JAD-160518
  2. IOS Press. “Mild cognitive impairment (MCI) detected with brain training game: A condition that often predates Alzheimer’s disease (AD), can be remotely detected through a self-administered virtual reality brain training game.” ScienceDaily. ScienceDaily, 24 February 2017. <www.sciencedaily.com/releases/2017/02/170224092544.htm>.