In this blog we will look at timely topics on the brain. Learn along with a copy from our book series, Healing the Brain. Get your copy today. A Thousand Moms offers workshops to the general public. These workshops are presented in clear, non-complicated language. In New York, Vermont and Massachusetts, please call 518 322-0607 or write to athousandmoms@yahoo.com.

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Alzheimer's, Parkinson's, and Huntington's diseases share common crucial feature

Finding suggests that treatment for one disease could work for the other two

Date:

May 23, 2017

Source:

Loyola University Health System

Summary:

A study has found that abnormal proteins found in Alzheimer's, Parkinson's and Huntington's diseases share a similar ability to cause damage when they invade brain cells. The finding suggests that an effective treatment for one neurodegenerative disease might work for other neurodegenerative diseases as well.

FULL STORY

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A Loyola University Chicago study has found that abnormal proteins found in Alzheimer's disease, Parkinson's disease, and Huntington's disease all share a similar ability to cause damage when they invade brain cells.

The finding potentially could explain the mechanism by which Alzheimer's, Parkinson's, Huntington's, and other neurodegenerative diseases spread within the brain and disrupt normal brain functions.

The finding also suggests that an effective treatment for one neurodegenerative disease might work for other neurodegenerative diseases as well.

The study by senior author Edward Campbell, PhD, first author William Flavin, PhD, and colleagues is published in the journal Acta Neuropathologica.

"A possible therapy would involve boosting a brain cell's ability to degrade a clump of proteins and damaged vesicles," Campbell said. "If we could do this in one disease, it's a good bet the therapy would be effective in the other two diseases."

Neurodegenerative diseases are caused by the death of neurons and other cells in the brain, with different diseases affecting different regions of the brain. Alzheimer's destroys memory, while Parkinson's and Huntington's affect movement. All three diseases are progressive, debilitating and incurable.

Previous research has suggested that in all three diseases, proteins that are folded abnormally form clumps inside brain cells. These clumps spread from cell to cell, eventually leading to cell deaths. Different proteins are implicated in each disease: tau in Alzheimer's, alpha-synuclein in Parkinson's and huntingtin in Huntington's disease.

The Loyola study focused on how these misfolded protein clumps invade a healthy brain cell. The authors observed that once proteins get inside the cell, they enter vesicles (small compartments that are encased in membranes). The proteins damage or rupture the vesicle membranes, allowing the proteins to then invade the cytoplasm and cause additional dysfunction. (The cytoplasm is the part of the cell that's outside the nucleus).

The Loyola study also showed how a cell responds when protein clumps invade vesicles: The cell gathers the ruptured vesicles and protein clumps together so the vesicles and proteins can be destroyed. However, the proteins are resistant to degradation. "The cell's attempt to degrade the proteins is somewhat like a stomach trying to digest a clump of nails," Campbell said.

Flavin said the finding that protein clumps associated with the three diseases cause the same type of vesicle damage was unexpected. Loyola researchers initially focused on alpha-synuclein proteins associated with Parkinson's disease. So they asked collaborator Ronald Melki, PhD, to send them samples of different types of alpha-synuclein. (To do the experiment in a blinded, unbiased manner, the Loyola researchers did not know which types of alpha-synuclein were which.) Melki, a protein researcher at the Paris-Saclay Institute of Neuroscience, is known for his ability to generate distinct types of alpha-synuclein. Without telling the Loyola researchers, Melki sent other types of proteins as well. This led to the surprise finding that tau and huntingtin proteins also can damage vesicles.

Campbell stressed the study's findings need to be followed up and confirmed in future studies.
The Loyola study is titled, "Endocytic vesicle rupture is a conserved mechanism of cellular invasion by amyloid proteins." It was supported by grants from the Michael J. Fox Foundation, Parkinson's Disease Foundation, Illinois chapter of the ARCS Foundation, Arthur J. Schmitt Foundation and other sources.

Campbell is an associate professor in the Department of Microbiology and Immunology at Loyola University Chicago Stritch School of Medicine. Flavin is a Loyola University Chicago MD/PhD student. Other co-authors are Zachary Green, Stratos Skarpathiotis, and Michael Chaney of Loyola University Chicago; Luc Bousset and Ronald Melki of the Paris-Saclay Institute of Neuroscience; and Yaping Chu and Jeffrey Kordower of Rush University Medical Center.

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Story Source:
Materials provided by Loyola University Health System.

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Ecstasy (Molly) for PTSD?

From the New York times comes news of possible use of Ecstasy for Post-Traumatic Stress Disorder, PTSD. In our new book, Healing the Brain, we take a close look at PTSD, what it is and how it affects people of all ages. 

F.D.A. Agrees to New Trials for Ecstasy as Relief for PTSD Patients

By DAVE PHILIPPS NOV. 29, 2016

C.J. Hardin, a veteran who served three tours in Iraq and Afghanistan, at a memorial in North Charleston, S.C. He is a patient in the study of MDMA, also known as Ecstasy, as a treatment for post-traumatic stress disorder. Credit Travis Dove for The New York Times

CHARLESTON, S.C. — After three tours in Iraq and Afghanistan, C. J. Hardin wound up hiding from the world in a backwoods cabin in North Carolina. Divorced, alcoholic and at times suicidal, he had tried almost all the accepted treatments for post-traumatic stress disorder: psychotherapy, group therapy and nearly a dozen different medications.

“Nothing worked for me, so I put aside the idea that I could get better,” said Mr. Hardin, 37. “I just pretty much became a hermit in my cabin and never went out.”

Then, in 2013, he joined a small drug trial testing whether PTSD could be treated with MDMA, the illegal party drug better known as Ecstasy.

“It changed my life,” he said in a recent interview in the bright, airy living room of the suburban ranch house here, where he now lives while going to college and working as an airplane mechanic. “It allowed me to see my trauma without fear or hesitation and finally process things and move forward.”

 

Based on promising results like Mr. Hardin’s, the Food and Drug Administration gave permission Tuesday for large-scale, Phase 3 clinical trials of the drug — a final step before the possible approval of Ecstasy as a prescription drug.

If successful, the trials could turn an illicit street substance into a potent treatment for PTSD.

Through a spokeswoman, the F.D.A. declined to comment, citing regulations that prohibit disclosing information about drugs that are being developed.

“I’m cautious but hopeful,” said Dr. Charles R. Marmar, the head of psychiatry at New York University’s Langone School of Medicine, a leading PTSD researcher who was not involved in the study. “If they can keep getting good results, it will be of great use. PTSD can be very hard to treat. Our best therapies right now don’t help 30 to 40 percent of people. So we need more options.”

But he expressed concern about the potential for abuse. “It’s a feel-good drug, and we know people are prone to abuse it,” he said. “Prolonged use can lead to serious damage to the brain.”

The Multidisciplinary Association for Psychedelic Studies, a small nonprofit created in 1985 to advocate the legal medical use of MDMA, LSD, marijuana and other banned drugs, sponsored six Phase 2 studies treating a total of 130 PTSD patients with the stimulant. It will also fund the Phase 3 research, which will include at least 230 patients...

Read out book and learn about PTSD.

 

Remembering a pioneer, Barbara Rich

At a holiday luncheon in New York City in the late 90s, Dana Foundation chairman David Mahoney was quite proud of his employees. We were making a big difference in the "Decade of the Brain" congressional project, he said.

At his behest, we posed for a photograph in the beautiful garden of the New York Academy of Sciences. I was in the photo, which Mr. Mahoney graciously signed personally and distributed to all those in the picture. Remember, he wrote, that you were there at the beginning.

Also among those gathered was Barbara Rich, in many ways the emotional and intellectual backbone of this group of which Mr. Mahoney was so proud.

Barbara was a renaissance woman. Kind, wicked smart, indefatigable, she eventually had a say in all parts of the Foundation, including the financial portfolio. We worked together on mutual projects, supporting each other. I learned a great deal more from her than the other way around. She was always striving to be a better person and gently encouraging me to do the same.

Anyone learning about the brain and concerned about a loved one--or themselves--suffering from depression, substance abuse, suicidal ideation or the myriad of other illnesses that can cripple individuals and minimize human potential, needs to thank Barbara Rich.

With great sadness that I learned of her passing earlier this month. I am too much at a loss for words to write more.

Thank you, Barbara. It was a great honor to know you and work alongside you.

Learn about the brain, here.