October 27, 2007 by mike.

by MT Bureau - October 27, 2007 - 0 comments
Tucson — A U.S. researcher says he thinks he knows why Parkinson’s patients treated with Deep Brain Stimulation often exhibit compulsive behaviors.

Michael Frank, of the Laboratory for Neural Computation and Cognition at The University of Arizona, and colleagues say DBS interferes with the brain’s innate ability to deliberate on complicated decisions.

DBS is a surgical treatment involving the implantation of a brain pacemaker, which sends electrical impulses to specific parts of the brain to treat disorders such as chronic pain, Parkinson’s disease and tremor. DBS implants affect the subthalamic nucleus part of the brain, which also modulates decision-making.

“This particular area of the brain is needed for what’s called a ‘hold-your-horses’ signal,” Frank said in a statement. “When you’re making a difficult choice, with a conflict between two or more options, an adaptive response for your system to do is to say ‘Hold on for a second. I need to take a little more time to figure out which is the best option.’”

This could be one explanation for why these patients develop gambling habits, Frank said.

The findings are published in the journal Science.

© 2007 United Press International.

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October 19, 2007 by mike.

Main Category: Alzheimer’s / Dementia News
Article Date: 11 Oct 2007 - 10:00 PDT

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In a finding that may lead to potential new treatments for diseases such as Alzheimer’s and Parkinson’s, researchers at the Picower Institute for Learning and Memory at MIT report an unexpected role in the brain for a well-known protein.

A study by Morgan H. Sheng, Menicon Professor of Neuroscience and a Howard Hughes Medical Institute investigator, and colleagues appearing in the Oct. 23 issue of Current Biology shows that the same protein that enables a yeast cell to bud into two daughter cells also helps neurons sprout the branch-like protrusions used to communicate with other neurons.

The work revolves around septins–proteins known since the 1970s to play an essential function in the process through which the cytoplasm of a single yeast cell divides. “In yeast, septin is localized exactly at the neck between the yeast mother cell and the bud or emerging daughter cell,” Sheng said. “Amazingly, we found septin protein localized at the base of the neck of neuronal dendritic spines and at the branchpoint of dendritic branches.”

Nine of the 14 septins found in mammals are found in the brain. One of them, Sept7, appears the most, but its role was unclear. Septins form long filaments and act as scaffolds, recruiting other proteins into their assigned roles of builders of the cell infrastructure.

While neurons don’t divide, they do form protrusions that eventually elongate into dendritic branches. Dendrites, from the Greek word for “tree,” conduct electrical stimulation from other neurons to the cell body of the neuron from which the dendrites project.

Electrical stimulation is transmitted via synapses, which are located at various points along the dendritic branches. Dendrites play a critical role in receiving these synaptic inputs. “Because dendritic spines are important for synaptic function and memory formation, understanding of septins may help to prevent the loss of spines and synapses that accompanies many neurodegenerative diseases,” said co-author Tomoko Tada, a postdoctoral associate in the Picower Institute. “Septin could be a potential target protein to treat these diseases.”

Moreover, in the cultured hippocampal neurons the researchers used in the study, septin was essential for normal branching and spine formation. An abundance of septin made dendrites grow and proliferate while a dearth of septin made them small and malformed.

“Boosting septin expression and function would enhance the stability of spines and synapses, and therefore be good for cognitive functions such as learning and memory,” Sheng said. His laboratory is now exploring ways to prevent septin degradation and loss.

In addition to Sheng and Tada, authors are MIT affiliates Alyson Simonetta and Matthew Batterton; Makoto Kinoshita of Kyoto University Graduate School of Medicine; and Picower postdoctoral associate Dieter Edbauer.

This work is supported by the National Institutes of Health and the RIKEN-MIT Neuroscience Research Center.

Written by Debbie Halber, Picower

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October 19, 2007 by mike.

Dr. Jay Adlersberg
(New York - WABC, October 12, 2007) - An interesting lesson shared on the Upper East Side. The wife of boxing legend Muhammad Ali spoke about her experience dealing with Parkinson’s disease.

Eyewitness News Dr. Jay Adlersberg was there and joins us with more.
Somehow the champ is always the champ, in the ring or years later with Parkinson’s disease.

Parkinson’s disease robs the body of smooth and coordinated muscle action and with time the illness can get worse. That’s where a patient’s caregiver or caregivers come in. For Muhammad Ali, it’s his wife Lonnie who is his main caregiver. Lonnie Ali has a very personal point of view on being a caregiver.

Today in Manhattan, Lonnie Ali spoke to a group of Parkinson’s patients and their caregivers as part of “Fight for More,” a program to spread information to the families of Parkinson’s patients.

“Hopefully this will inspire them and give them resources they need and give them hope,” said Parkinson’s caregiver Lonnie Ali.

Part of that hope is Dr. Warren Olanow, a researcher in the illness. Despite advances in treatments, it’s the human partnership that’s critical.

“Parkinson’s disease is a two person disease and both patient and caregiver require attention,” said Dr. Warren Olanow at Mt. Sinai Medical Center.

Two people like Kate and Gary Oberlin, Gary recently had brain surgery for Parkinson’s and though his muscle skills are better, he’s still a challenge.

“One day he’ll be perfect and the next day he’ll be off or have mood changes on the surface. It’s not predictable,” said Kate Oberlin, caregiver for Gary. “So, it’s kind of the unpredictability of the disease,”

Perhaps this caregiver tip sheet will help make things more predictable. It talks about things like keeping active, keeping a sense of humor and taking care of yourself.

Though there is a lot to take care about the health of Parkinson’s patients, it’s the caregiver’s health that is an issue. It takes two strong bodies to fight the disease.

“I sprained my foot and I didn’t see a doctor. I kept putting it off and off,” said Lonnie Ali. “It is important that if something happens, you don’t delay it.”

Gary Oberlin says that sometimes he gets depressed over how much attention his wife has to pay to him because of his Parkinson’s. It’s obvious there are emotional issues that the program “Fight for More” can provide resources for as well.

The caregiver tip sheet is based on Lonnie’s 20 years of being a caregiver for her husband.

For more information, visit Fight for More website

(Copyright 2007 WABC-TV. All Rights Reserved.)

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October 19, 2007 by mike.

Monday, October 08, 2007

ROCHESTER, Minn. — Immediate relatives of people who have Parkinson’s disease are at greater risk of developing cognitive impairment or dementia than people who have no first-degree relatives (brother, sister, mother, father, son or daughter) with Parkinson’s disease, according to a new study by Mayo Clinic. The risk is particularly increased for relatives of patients who developed Parkinson’s disease before age 67.

Significance of the Mayo Clinic Research

This is one of the first large population-based studies to show that Parkinson’s disease and cognitive impairment or dementia may share familial factors that make a person susceptible to developing one or both disorders. In addition, the study is a major methodological departure from previous attempts to study the risk of cognitive impairment or dementia in families with Parkinson’s disease. It is based on the “family study” method. Researchers assessed each relative separately for cognitive status instead of using only one family member to provide information for the full family. The Mayo Clinic report appears in the October 2007 issue of the journal Archives of Neurology (http://archneur.ama-assn.org/).

Walter Rocca, M.D., is lead author of the study and a Mayo Clinic neurologist and epidemiologist who specializes in the study of neurological diseases in the population. “Because the evidence for increased risk of dementia in relatives of patients with Parkinson’s disease was conflicting, we set out to clarify it,” says Dr. Rocca. “We show that cognitive impairment or dementia may share familial susceptibility factors with Parkinson’s disease — which means that if a person is susceptible to developing Parkinson’s disease, the same susceptibility factors may predispose the person to cognitive impairment or dementia.” Dr. Rocca emphasizes that the familial susceptibility factors may be genetic or may be nongenetic, such as shared diet in the family. Further research is needed to determine susceptibility factors.

About the study

The Mayo Clinic team studied: 1. 1,019 first-degree relatives of 162 patients with Parkinson’s disease from Olmsted County, Minn., where Mayo Clinic’s Minnesota campus is located 2. 858 first-degree relatives of 147 “matched controls” from the same Olmsted County population — the controls were similar in age and sex to the patients in the first group, but did not have Parkinson’s disease 3. 2,716 first-degree relatives of 411 patients with Parkinson’s disease who were referred to Mayo Clinic from a broader area, including Minnesota, Iowa, Wisconsin, North Dakota and South Dakota

For each group, researchers administered via telephone a cognitive test to relatives. If a relative was deceased or unavailable, researchers administered via telephone a brief dementia questionnaire to a close family member. If the family member reported that the relative had dementia, Mayo Clinic researchers obtained a copy of the medical record to confirm the diagnosis. Researchers had access to extensive documentation of dementia from medical records archived at Mayo Clinic. The sample group studied included both patients with Parkinson’s disease who lived in the local county and those who were referred to Mayo Clinic.

Several intriguing leads prompted the researchers to hypothesize the existence of familial shared susceptibility factors for Parkinson’s disease and cognitive impairment or dementia. One was that dementia tends to occur in patients who have Parkinson’s disease, and there is some suggestion it may be due to shared susceptibility genetic variations such as those in the apolipoprotein E gene. Another lead was that both conditions cause lesions on the brain that disrupt normal brain function. In Alzheimer’s disease, these lesions are called plaques and tangles. In Parkinson’s disease, the lesions are called Lewy bodies. It is thought that these brain lesions may share common risk factors.

About Parkinson’s disease

Parkinson’s disease is a chronic, progressive movement disorder typically seen in people over age 50 and affecting approximately two in 100 people. The diagnosis of Parkinson’s disease requires the presence of at least two of the following symptoms: tremors while at rest, rigidity of the muscles, loss of postural control, and slowed movements such as a slow gait. “Parkinsonism” is the term used to describe patients who have some of these symptoms but do not completely fit the diagnosis. Parkinson’s disease symptoms are caused by the death or damage to key brain cells in the part of the brain known as the nigrostriatal dopamine system, which is involved in coordinating movements. The exact cause of the damage to that system is not known.

Collaboration and support

Other members of the Mayo Clinic team included: James Bower, M.D.; J. Eric Ahlskog, M.D., Ph.D.; Alexis Elbaz, M.D., Ph.D.; Brandon Grossardt; Shannon K. McDonnell; Daniel J. Schaid, Ph.D.; and Demetrius Maraganore, M.D. Their work was supported by two grants from the National Institutes of Health.

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