Transcranial lights are the way to go.

Here’s a new journal article from the Journal of Alzheimer’s Disease. I’m a co-author, but don’t let that get in the way.

This article looks at the animal and clinical evidence for the use of transcranial and intracranial red and near infrared light devices. There is a lot of detailed information, including and in-depth description of the effect of transcranial red and near infrared lights in people with Parkinson’s disease.

As for which is best – intracranial or transcranial? The verdict is that neither is best on its own. The best is having both working together. It makes sense, having light shining from inside and outside the brain.

Alas, you might be waiting a while before you get access to an intracranial light implant (think DBS with a 670nm LED light), but you can use transcranial lights right now. You can make your own (instructions are here) or look at the Duo Coronet (link is here) .

Meanwhile, have a read…

Reference

Johnstone DM, Hamilton C, Gordon LC, Moro C, Torres N, Nicklason F, Stone J, Benabid AL, Mitrofanis J. Exploring the Use of Intracranial and Extracranial (Remote) Photobiomodulation Devices in Parkinson’s Disease: A Comparison of Direct and Indirect Systemic Stimulations. J Alzheimers Dis. 2021;83(4):1399-1413. doi: 10.3233/JAD-210052. PMID: 33843683.

Mitochondria have a social-life!

The discoveries about mitochondria continue to grow.

A while back, it became clear that many neurodegenerative diseases, especially Parkinson’s and Alzheimer’s, resulted from the cell batteries, the mitochondria, failing to properly power up the cell. This results in the cell being unable to do its job, for example making dopamine. It also results in the early death of the cell.

In 2019 came the stunning news that mitochondria are nomadic. They pop out of cells, plunge into the bloodstream and whizz around, then get out, metaphorically towel themselves dry and pop back into a different cell – possibly in a completely different part of the body.

This ability raised the question of what controls the mitochondrial migration. There must be some signalling system making this happen. One has visions of King Mito barking out orders to mitochondrial minions, who scurry around with their clipboards and spreadsheets…

The signalling system is the next big thing for scientists to understand. It offers vast opportunities for potential treatments and prevention strategies.

Now comes the news that mitochondria act like social creatures. The cosy up to each other, fuse together, split apart, and appear to communicate with each other. Absolutely fascinating!

Here’s a link to a wonderful article in Qantamagazine. It describes very beautifully the implication of a review paper by Martin Picard and Carmen Sandi, who were the first to describe this new feature of mitochondrial behaviour.

Reference:

Martin Picard, Carmen Sandi,The social nature of mitochondria: Implications for human health,
Neuroscience & Biobehavioral Reviews, Volume 120,
2021,Pages 595-610,ISSN 0149-7634,
https://doi.org/10.1016/j.neubiorev.2020.04.017.

Exercise and sleep in Parkinson’s

Hot off the research press is a journal article with a self-explanatory title: Effects of exercise on sleep in neurodegenerative disease.

It starts by summarising the main things that affect sleep in people with Parkinson’s, Alzheimer’s and other neurodegenerative diseases as being:

  1. damage to the sleep-wake system in the brain, that affects the circadian rhythm and disrupts normal sleeping and waking patterns; and
  2. “secondary mechanisms” which include a raft of things like medication side effects, having to get up to the toilet during the night, poor sleep “hygiene”, sleep-related breathing disorders, and the environment in which you try to sleep.
Continue reading “Exercise and sleep in Parkinson’s”

Movement and Molecules

Below is an excellent article written by Gretchen Reynolds, first published in the New York Times and reprinted in The Age on 1 December 2020. Reynolds describes new research into the effect of movement on molecules in the blood and what that might mean for quality of life and length of life.

If you’ve ever thought that exercise of any degree or duration is over-rated, then this is the article for you: Link

Thanks to John Moeses Bauan from Unsplash for this gorgeous photo.

Mitochondria & Alzheimer’s

Alzheimer’s disease researchers have had to do a complete revision of thinking. For decades, the focus has been on getting rid of an abnormal protein, called amyloid, that plonks itself  in the brains of people with Alzheimer’s.

It was a reasonable hypothesis. Amyloid and Alzheimer’s seem to go together, so it seemed logical that in getting rid of amyloid proteins, Alzheimer’s would be cured.

Billions of dollars later, and despite lots of trials with amyloid-chewing drugs, it seems that amyloid is not the culprit.

Q: So what is the culprit?
A: Lots of things, especially mitochondria, the batteries that power our cells.

It’s not a surprise that miserable mitochondria are heavily involved in Alzheimer’s. More and more evidence is showing that moping mitochondria appear in many different diseases. It seems that cell battery management is critical, which makes a lot of sense.

The number of articles linking Alzheimer’s and mitochondria are increasing, and the hope is to find pharmaceutical solutions. That’s good, but there is a solution already in place. And one without side effects.

Photobiomodulation acts on the cell mitochondria, the cell batteries, and boosts the cell activity, stimulates the cell nucleus to start making new cells, opens up the blood vessels and stimulates the blood vessels to sprout more branches. We know from research, case studies and observations of people with Alzheimer’s disease that red and near infrared transcranial lights used daily can improve memory, judgement, attention and concentration, mood, apathy, sleep quality, fatigue, not to mention increasing enjoyment of life.

It would be so good if some of those billions of dollars for Alzheimer’s research would include more work on photobiomodulation.

References:
1. Stojakovic, A., Trushin, S., Sheu, A. et al. Partial inhibition of mitochondrial complex I ameliorates Alzheimer’s disease pathology and cognition in APP/PS1 female mice. Commun Biol 4, 61 (2021). https://doi.org/10.1038/s42003-020-01584-y Link.
2. Bell, Simon M.; Barnes, Katy; De Marco, Matteo; Shaw, Pamela J.; Ferraiuolo, Laura; Blackburn, Daniel J.; Venneri, Annalena; Mortiboys, Heather. 2021. “Mitochondrial Dysfunction in Alzheimer’s Disease: A Biomarker of the Future?” Biomedicines 9, no. 1: 63. Link

Thanks to Mika Baumeister on Unsplash for the wonderful image of a battery.