Bright Light Therapy in Parkinson's Disease: An Overview of the Background and Evidence

Better than yet another diet or pill....

Worth a try.

http://www.infoplease.com/ipa/A0001769.html

Lat/Long for cities of world. Somewhere there are dusty records of the first artificial lighting for each. That's the easy part. The tricky stuff is the way PD rates evolved.

Better than yet another diet or pill....

Worth a try.[/QUOTE]

Laura,

I really like my custom blue lensed glasses - they definitely take an edge off and settle dk for me.

Thank you for posting this.
Insomnia was something that I've been dealing with for over 20 years. After diagnosis, I feel as if it were an early symptom. Then some days I wonder if it was the cause?!?!
I found it interesting that they mention melatonin as interfering with the dopamine pathways, and making motor symptoms worse.
I've been taking melatonin nightly for years. It really helps me sleep but maybe it's time to switch to something else!
I had read previously that melatonin was supposed to be a good thing for people with PD.

Melatonin is only good for you up to 2 weeks then becomes detrimental over the long haul. I have a complete light therapy (IR) set, the head thing and the pads for the back etc with no result for me. Also used the "Pen" with no effect at all. recommend you don't spend the money.


Peace,
BP with Pd since 2003 no meds only naturally.

A new article in science daily today (turkey/trytophan- day) caught my attention

http://www.sciencedaily.com/releases...1125125352.htm

I am going to revisit melatonin and sunlight - maybe raise a melatonin dosage to 10mg. from very rare and sporatic use.

Broken Cellular 'Clock' Linked to Brain Damage


Nov. 25, 2013 — A new discovery may help explain the surprisingly strong connections between sleep problems and neurodegenerative conditions such as Alzheimer's disease. Sleep loss increases the risk of Alzheimer's disease, and disrupted sleeping patterns are among the first signs of this devastating disorder.
Scientists at Washington University School of Medicine in St. Louis and the University of Pennsylvania have shown that brain cell damage similar to that seen in Alzheimer's disease and other disorders results when a gene that controls the sleep-wake cycle and other bodily rhythms is disabled.
The researchers found evidence that disabling a circadian clock gene that controls the daily rhythms of many bodily processes blocks a part of the brain's housekeeping cycle that neutralizes dangerous chemicals known as free radicals.
"Normally in the hours leading up to midday, the brain increases its production of certain antioxidant enzymes, which help clean up free radicals," said first author Erik Musiek, MD, PhD, assistant professor of neurology at the School of Medicine. "When clock genes are disabled, though, this surge no longer occurs, and the free radicals may linger in the brain and cause more damage."
Musiek conducted the research in the labs of Garret FitzGerald, MD, chairman of pharmacology at the University of Pennsylvania, and of David Holtzman, MD, the Andrew B. and Gretchen P. Jones Professor and head of the Department of Neurology at Washington University School of Medicine, who are co-senior authors.
The study appears Nov. 25 in The Journal of Clinical Investigation.
Musiek studied mice lacking a master clock gene called Bmal1. Without this gene, activities that normally occur at particular times of day are disrupted.
"For example, mice normally are active at night and asleep during the day, but when Bmal1 is missing, they sleep equally in the day and in the night, with no circadian rhythm," Musiek said. "They get the same amount of sleep, but it's spread over the whole day. Rhythms in the way genes are expressed are lost."
FitzGerald uses mice lacking Bmal1 to study whether clock cells have links to diabetes and heart disease. He has shown that clock genes influence blood pressure, blood sugar and lipid levels.
Several years ago, Musiek, who at the time was a neurology resident at the University of Pennsylvania, and FitzGerald decided to investigate how knocking out Bmal1 affects the brain. Holtzman, who has published pioneering work on sleep and Alzheimer's disease, encouraged Musiek to continue and expand these studies when he came to Washington University as a postdoctoral fellow.
In the new study, Musiek found that as the mice aged, many of their brain cells became damaged and did not function normally. The patterns of damage were similar to those seen in Alzheimer's disease and other neurodegenerative disorders.
"Brain cell injury in these mice far exceeded that normally seen in aging mice," Musiek said. "Many of the injuries appear to be caused by free radicals, which are byproducts of metabolism. If free radicals come into contact with brain cells or other tissue, they can cause damaging chemical reactions."
This led Musiek to examine the production of key antioxidant enzymes, which usually neutralize and help clear free radicals from the brain, thereby limiting damage. He found levels of several antioxidant proteins peak in the middle of the day in healthy mice. However, this surge is absent in mice lacking Bmal1. Without the surge, free radicals may remain in the brain longer, contributing to the damage Musiek observed.
"We're trying to identify more specifics about how problems in clock genes contribute to neurodegeneration, both with and without influencing sleep," Musiek said. "That's a challenging distinction to make, but it needs to be made because clock genes appear to control many other functions in the brain in addition to sleeping and waking."