Know the signs of Alzheimer’s disease

November 18, 2017

We have all occasionally experienced the frustration of misplacing our car keys, forgetting someone’s name or losing track of what we wanted to say. Some small memory lapses are a normal part of the aging process and are not cause for alarm.

But when someone forgets the names of family members or what the car keys are for, it may be a sign of an underlying problem: Alzheimer’s disease.

Alzheimer’s is a progressive disease that attacks the brain and affects memory, thinking and behavior. Approximately 5.4 million Americans have the disease, according to the Alzheimer’s Association.

Recognizing the symptoms

The main sign of the disease is dementia (loss of memory and intellectual function) so severe that it interferes with work and social activities. Problems usually occur in adults middle-aged and older.

According to the association, other signs of the disease include:

• Difficulty performing familiar tasks.
• Problems with language.
• Disorientation in time and place.
• Problems with abstract thinking.
• Misplacing things.
• Poor or decreased judgment.
• Changes in personality, mood or behavior.
• Loss of initiative.

Diagnosing the disease

There’s a definite challenge in diagnosing Alzheimer’s. First, there is no single screening test. And the disease can only be diagnosed definitively after death, by an examination of brain tissue.

Further, other disorders—such as depression, brain tumors, Parkinson’s disease, stroke and thyroid disease—have dementia symptoms similar to Alzheimer’s. In fact, doctors make a probable diagnosis of the disease by eliminating other possible causes for the symptoms.

A person experiencing dementia needs a complete medical and neurological exam, according to the association. The disease affects people in many different ways, making it difficult to predict how it will progress in any 1 individual.

Reaching out for help

While there is still no cure for Alzheimer’s, many of the conditions that cause dementia are treatable. If your loved one shows signs that could indicate Alzheimer’s, the association suggests that you schedule an evaluation with your doctor.

If your loved one is diagnosed with Alzheimer’s, remember that there is support and help available. The Alzheimer’s Association has local chapters nationwide, which provide services and programs to families affected by the disease. For information, call 800.272.3900.

http://www.villages-news.com/know-signs-alzheimers-disease/

I'm abused for being drunk... but I have Parkinson's disease

November 17, 2017  Tom Nellist, Reporter

Dave Trinder suffers from Parkinson's disease and is raising awareness about the condition after receiving abusive comments from the public

A PARKINSON’S disease sufferer from Cirencester has opened up about the abusive comments he receives on a daily basis, as people wrongly mistake him for being drunk.

Dave Trinder, who has lived with the condition for more than 12 years, says he is hoping to change people’s misconceptions of Parkinson’s, after growing frustrated of the hurtful comments.

The 60-year-old received pioneering deep brain stimulation surgery five years ago meaning he has full control of his hands and no longer suffers from tremors, but his feet often claw up and he struggles with walking and balance.

This has led to people mistaking his staggered walking for being drunk and in the past people have shouted comments such as ‘I’ll have a pint of what you’re on mate’ at him.

“I reply with ‘You wouldn’t want a pint of Parkinson’s would you?’”, said Dave.

“Once I say Parkinson’s people say they are sorry but probably everyone who makes these comments has got someone with dementia or a neurological illness in their family.

“Most days I go out the door someone says something to me or I get looks and sneers if I’m struggling with my walking.

“How would they feel if their family members were being ridiculed like that?

“It’s human nature, I understand and I’m not angry, I’m just annoyed.

"There’s no point in being angry, they are just being ignorant.”

Dave said the comments can come from anybody.

Often it is young men who are drunk themselves but two weeks ago he was walking along Cricklade Street when he heard a mother say to her young children, “Get away from him”.

Dave, whose nephew Henry plays for Gloucester rugby club, has organised fundraising events for Parkinson’s UK and in September his entertainment night at the Bingham Hall raised more than £9,000.

Earlier this week, Dave had his five year appraisal for the brain stimulation surgery.

In 2012, he was one of just 40 people in eight countries to participate in the trial. 

“I’ve always referred to the operation as giving my life back, instead of being too scared to go outside.

"It’s is a degenerative illness and the last year has seen the biggest change.

"I’ll go downhill but I don’t know how quickly, a year ago I didn’t have a problem with my speech but sometimes now I can’t get the words out, that’s very frustrating.”

http://www.wiltsglosstandard.co.uk/news/15665783.Man_with_Parkinson_s_speaks_out_after_receiving_abusive_comments/

FoxFeed Blog: Building the Base of Movement Disorder Specialists

Posted by  Rachel Dolhun, MD, November 16, 2017

Editor's Note: For more Foundation news, research updates and tips on living well with Parkinson's, read the Fall/Winter 2017 edition of The Fox Focus, our biannual newsletter.

People with Parkinson's and their loved ones know firsthand the importance of a good doctor. Throughout life with Parkinson's disease (PD), patients need a physician who can adjust sometimes-complex medication regimens, incorporate newly available therapies, and, if necessary, call on other experts, such as physical and speech therapists, to round out a care team.

Movement disorder specialists -- neurologists with extra training in Parkinson's -- have the knowledge and experience necessary to offer this holistic and individualized care. But not everyone with PD sees a movement disorder specialist because there aren't enough of them. Lack of funding for fellowship training and limited exposure to the specialty during residency hold doctors back from pursuing movement disorder careers.

To meet current and growing needs of Parkinson's care and research, a broad, global base of movement disorder specialists is key. Drawing on our "if not us, then who" attitude, The Michael J. Fox Foundation (MJFF), with longtime partner the Edmond J. Safra Foundation, is investing in two initiatives to fill the pipeline of Parkinson's experts and secure the field's future. 

The Edmond J. Safra Fellowship in Movement Disorders aims to bridge the funding gap to train clinician-researchers who can directly link patients to the scientific developments necessary for new and better therapies. Annually, this program selects five academic institutions from around the world to train a movement disorder specialist over a two-year period -- as of early 2018, a total of 20 fellows will be supported. 

The MDS-PAS Movement Disorders School for Neurology Residents provides physicians in training a two-day immersion in Parkinson's and other movement disorders. At a period when these doctors are contemplating career paths, the course offers comprehensive education and interaction with internationally renowned movement disorder experts. Over the past two years, 150 residents from across the world and spanning all three years of neurology training have attended. The 2018 program hopes to host 100 new students. 

As more therapies move into testing and to market, it is critical to have a workforce of trained specialists who can optimize care, advance research and connect the dots between the two. Investing in the next generation of movement disorder specialists will have long-term gains for the entire Parkinson's community.

https://www.michaeljfox.org/foundation/news-detail.php?building-the-base-of-movement-disorder-specialists

Deep Brain Stimulation Surgery Works Better If Patients Are Asleep, Study Suggests

NOVEMBER 17, 2017   BY MAGDALENA KEGEL

Deep brain stimulation surgery, used to treat the effects of Parkinson’s disease, is performed better when patients are asleep rather than awake, researchers from the Oregon Health & Science University (OHSU) suggested in a recent study comparing the two surgical settings.

The study could influence how the procedure is performed around the world, as patients are given the opportunity to reduce their symptoms without the need for experiencing a six-hour brain surgery while awake.

“It doesn’t take a rocket scientist, or a brain surgeon, to tell you that patients prefer it,” Kim Burchiel, MD, professor of neurosurgery at the OHSU School of Medicine and senior study author, said in a press release.

The practice of keeping patients awake during this type of surgery stems from the need to accurately place electrodes in the brain of a Parkinson’s patient. These electrodes stimulate nerve cells to reduce movement symptoms of the disease, but they need to be precisely located to do their work.

Until now, the gold standard for deep brain stimulation surgery has been the use of so-called microelectrodes. These map out the boundaries of the targeted brain structure. Initial measurements are also used to assess if the stimulation is effective or if it causes side effects before the surgery is completed.

Better brain imaging methods have made it possible to identify the correct brain structure without the need for placing these microelectrodes. This, in turn, allows patients to be asleep during the procedure.

In the study, “Clinical outcomes of asleep vs awake deep brain stimulation for Parkinson disease,” OHSU researchers compared the outcomes of patients who had the procedure while asleep with those who had traditional surgery while awake in a clinical trial (NCT01703598).

In 2011, OHSU switched to the new procedure and compared outcomes among patients operated on in 2010 with those who had electrodes implanted later. Burchiel performed all 69 surgeries in the study.

The results, published in the journal Neurology, suggested that it is better for patients to sleep through the surgery.

Additionally, traditional forms of deep brain stimulation surgery often cause patients to lose speech fluency. Matthew Brodsky, MD, an associate professor of neurology at the OHSU School of Medicine and medical director of OHSU’s deep brain stimulation program, believes that this side effect could be related to the use of microelectrodes.

Using microelectrodes, surgeons need to perforate the brain twice — once with the microelectrodes and again to position the electrode and battery pack that will remain in the brain.

“Patients undergoing asleep-DBS [deep brain stimulation] had improved speech versus patients undergoing awake DBS, whose speech fluency predictably worsened,” said Brodsky, who is the lead author of the study.

Meanwhile, improvements in Parkinson’s symptoms were similar in the two groups.

“If the patient’s outcome is not better or at least the same as awake-DBS, then you shouldn’t be doing it,” Burchiel said. “This article is really a watershed because we’re in a position to say, why would you ever do an awake surgery if you can get the same results or better when the patients are asleep – and the patients’ satisfaction is dramatically better?”

In an accompanying editorial, two scientists from the U.K. concluded that the study shows that the use of imaging in asleep patients will reduce risks without mitigating outcomes. They also underscored that the asleep procedure is faster and cheaper than the method used in awake patients.

Instead, the use of microelectrodes should be reserved for use in a research setting, they wrote.

While asleep deep brain stimulation surgery is not performed at many clinics outside of OHSU, Burchiel thinks his clinic will soon be joined by others as neurosurgeons realize the benefits of the newer procedure.

https://parkinsonsnewstoday.com/2017/11/17/parkinsons-disease-outcomes-deep-brain-stimulation-surgery-better-sleeping-patients/

Brain Activity Buffers Against Worsening Anxiety

NEUROSCIENCE NEWS  NOVEMBER 17, 2017
Source: Duke University.

Summary: It may be possible to buffer against developing depression and anxiety by boosting brain activity in areas associated with problem solving, a new study reports.

Individuals whose brains exhibit a high response to threat in the amygdala (left) and a low response to reward in the ventral striatum (middle) are more at risk of developing symptoms of anxiety and depression over time. The new study shows that these at-risk individuals were less likely to develop anxiety if they also had high activity in the dorsolateral prefrontal cortex (right).NeuroscienceNews.com image is credited to Matthew Scult, Duke University.

Boosting activity in brain areas related to thinking and problem-solving may also buffer against worsening anxiety, suggests a new study by Duke University researchers.

Using non-invasive brain imaging, the researchers found that people at-risk for anxiety were less likely to develop the disorder if they had higher activity in a region of the brain responsible for complex mental operations. The results may be a step towards tailoring psychological therapies to the specific brain functioning of individual patients.

“These findings help reinforce a strategy whereby individuals may be able to improve their emotional functioning — their mood, their anxiety, their experience of depression — not only by directly addressing those phenomena, but also by indirectly improving their general cognitive functioning,” said Ahmad Hariri, a professor of psychology and neuroscience at Duke. The results are published Nov. 17 in the journal Cerebral Cortex.

Previous findings from Hariri’s group show that people whose brains exhibit a high response to threat and a low response to reward are more at risk of developing symptoms of anxiety and depression over time.

In the current work, Hariri and Matthew Scult, a clinical psychology graduate student in the department of psychology and neuroscience at Duke, wanted to investigate whether higher activity in a region of the brain called the dorsolateral prefrontal cortex could help shield these at-risk individuals from future mental illness.

“We wanted to address an area of understanding mental illness that has been neglected, and that is the flip side of risk,” Hariri said. “We are looking for variables that actually confer resiliency and protect individuals from developing problems.”

The dorsolateral prefrontal cortex is our brain’s “executive control” center, helping us focus our attention and plan complex actions. It also plays a role in emotion regulation, and well-established types of psychotherapy, including cognitive behavioral therapy, engage this region of the brain by equipping patients with strategies to reframe or re-evaluate their emotions.

The team drew on data from 120 undergraduate students who participated in the Duke Neurogenetics Study. Each participant completed a series of mental health questionnaires and underwent a type of non-invasive brain scan called functional Magnetic Resonance Imaging (fMRI) while engaged in tasks meant to activate specific regions of the brain.

The researchers asked each participant to answer simple memory-based math problems to stimulate the dorsolateral prefrontal cortex. Participants also viewed angry or scared faces to activate a region of the brain called the amygdala, and played a reward-based guessing game to stimulate activity in the brain’s ventral striatum.

Scult was particularly interested in “at-risk” individuals with the combination of high threat-related activity in the amygdala and low reward-related activity in the ventral striatum. By comparing participants’ mental health assessments at the time of the brain scans, and in a follow-up occurring on average seven months later, he found that these at-risk individuals were less likely to develop anxiety if they also had high activity in the dorsolateral prefrontal cortex.

“We found that if you have a higher functioning dorsolateral prefrontal cortex, the imbalance in these deeper brain structures is not expressed as changes in mood or anxiety,” Hariri said.

The dorsolateral prefrontal cortex is especially skilled at adapting to new situations, the researchers say. Individuals whose brains exhibit the at-risk signatures may be more likely to benefit from strategies that boost the brain’s dorsolateral prefrontal activity, including cognitive behavioral therapy, working memory training, or transcranial magnetic stimulation (TMS).

But, the researchers warn, the jury is still out on whether many brain-training exercises improve the overall functioning of the dorsolateral prefrontal cortex, or only hone its ability to complete the specific task being trained. Additional studies on more diverse populations are also needed to confirm their findings.

“We are hoping to help improve current mental health treatments by first predicting who is most at-risk so that we can intervene earlier, and second, by using these types of approaches to determine who might benefit from a given therapy,” Scult said.

ABOUT THIS NEUROSCIENCE RESEARCH ARTICLE

Source: Kara Manke – Duke University

Publisher: Organized by NeuroscienceNews.com.

Image Source: NeuroscienceNews.com image is credited to Matthew Scult, Duke University.

Original Research: Abstract for “Prefrontal Executive Control Rescues Risk for Anxiety Associated with High Threat and Low Reward Brain Function” by Matthew A Scult, Annchen R Knodt, Spenser R Radtke, Bartholomew D Brigidi, and Ahmad R Hariri in Cerebral Cortex. Published online November 17 2017 doi:10.1093/cercor/bhx304

Abstract

Prefrontal Executive Control Rescues Risk for Anxiety Associated with High Threat and Low Reward Brain Function

Compared with neural biomarkers of risk for mental illness, little is known about biomarkers of resilience. We explore if greater executive control-related prefrontal activity may function as a resilience biomarker by “rescuing” risk associated with higher threat-related amygdala and lower reward-related ventral striatum activity. Functional MRI was used to assay baseline threat-related amygdala, reward-related ventral striatum, and executive control-related prefrontal activity in 120 young adult volunteers. Participants provided self-reported mood and anxiety ratings at baseline and follow-up. A moderation model revealed a significant three-way interaction wherein higher amygdala and lower ventral striatum activity predicted increases in anxiety in those with average or low but not high prefrontal activity. This effect was specific to anxiety, with the neural biomarkers explaining ~10% of the variance in change over time, above and beyond baseline symptoms, sex, age, IQ, presence or absence of DMS-IV diagnosis, and both early and recent stress. Our findings are consistent with the importance of top-down executive control in adaptive regulation of negative emotions, and highlight a unique combination of neural biomarkers that may identify at-risk individuals for whom the adoption of strategies to improve executive control of negative emotions may prove particularly beneficial.

“Prefrontal Executive Control Rescues Risk for Anxiety Associated with High Threat and Low Reward Brain Function” by Matthew A Scult, Annchen R Knodt, Spenser R Radtke, Bartholomew D Brigidi, and Ahmad R Hariri in Cerebral Cortex. Published online November 17 2017 doi:10.1093/cercor/bhx304

http://neurosciencenews.com/anxiety-brain-activity-7973/

Astrocytes Linked to Alzheimer’s Disease

NEUROSCIENCE NEWS  NOVEMBER 17, 2017
Source: University of Eastern Finland.

Summary: Researchers have discovered a direct association between astrocytes and Alzheimer’s disease. In a new study, researchers report astrocytes in the brains of Alzheimer’s patients produced significantly more amyloid beta than astrocytes in the brains of people without the disease.

Representative immunocytochemistry images of astrocytes from control, AD, and isogenic control lines matured with CNTF and BMP4 for 7 days, stained for S100β (green) and GFAP (red). Nuclei are stained with Hoechst. Scale bars, 50 μm. NeuroscienceNews.com image is credited to Oksanen et al./Stem Cell Reports.

Astrocytes, the supporting cells of the brain, could play a significant role in the pathogenesis of Alzheimer’s disease (AD), according to a new study from the University of Eastern Finland. This is the first time researchers discovered a direct association between astrocytes and AD. Published in Stem Cell Reports, the study investigated the brain cell function of familial AD patients by using stem cell technologies.

Alzheimer’s disease is the most common dementia type, with no treatment to slow down the progression of the disease currently available. The mechanisms of AD are poorly understood, and drug therapy has focused on restoring the normal function of neurons and microglia, i.e. cells mediating brain inflammation. The new study shows that astrocytes, also known as the housekeeping cells of the brain, promote the decline of neuron function in AD. The findings suggest that at least some familial forms of AD are strongly associated with irregular astrocyte function, which promotes brain inflammation and weakens neurons’ energy production and signalling.

Astrocytes are important brain cells, as they support neurons in many different ways. Astrocytes are responsible, for example, for the energy production of the brain, ion and pH balance, and they regulate synapse formation, the connections between neurons. Recent evidence suggests that human astrocytes are very different from their rodent counterparts and thus, it would be essential to use human cells to study human diseases.

However, the availability of human astrocytes for research has been very limited. The study carried out at the University of Eastern Finland used the induced pluripotent stem cell technology, which enables the generation of pluripotent stem cells from human skin fibroblasts. These induced stem cells can then be further differentiated to brain cells, e.g. neurons and astrocytes, with the same genetic background as the donor had.

The study compared astrocytes from familial AD patients carrying a mutation in the presenilin 1 gene to astrocytes from healthy donors, and the effects of these cells on healthy neurons were also analysed.

The researchers found out that astrocytes in patients with Alzheimer’s disease produced significantly more beta-amyloid than astrocytes in persons without AD. Beta-amyloid is a toxic protein that is known to accumulate in the brains of AD patients. 

In addition, AD astrocytes secreted more cytokines, which are thought to mediate inflammation. AD astrocytes also showed alterations in their energy metabolism which likely led to increased production of reactive oxygen species and reduced production of lactate, an important energy substrate for neurons. Finally, when astrocytes were co-cultured with healthy neurons, AD astrocytes caused significant changes on the signalling activity of neurons when compared to healthy astrocytes.

This study was the first to show that astrocytes in patients with Alzheimer’s disease manifest many pathological changes typical of AD. Astrocytes could thus play a key role in the early stages of the disease and changes in the function of these cells could lead to neurodegeneration.

“The induced pluripotent stem cells we used in this study proved to be extremely useful in disease modelling, and they could offer an excellent platform for drug discovery and testing new therapeutic targets for Alzheimer’s disease in the future,” says Early Stage Researcher Minna Oksanen, the lead author of the study.

ABOUT THIS NEUROSCIENCE RESEARCH ARTICLE

Funding: This study was conducted at the University of Eastern Finland, A.I. Virtanen Institute for Molecular Sciences, in Professor Jari Koistinaho’s research group in collaboration with the University of Turku and the University of Wisconsin-Madison. The research consortium was supported by JPND-CO-FUND funding via the Academy of Finland.

Source: Minna Oksanen – University of Eastern Finland

Publisher: Organized by NeuroscienceNews.com.

Image Source: NeuroscienceNews.com image is credited to Oksanen et al./Stem Cell Reports..

Original Research: Full open access research for “PSEN1 Mutant iPSC-Derived Model Reveals Severe Astrocyte Pathology in Alzheimer’s Disease” by Minna Oksanen, Andrew J. Petersen, Nikolay Naumenko, Katja Puttonen, Šárka Lehtonen, Max Gubert Olivé, Anastasia Shakirzyanova, Stina Leskelä, Timo Sarajärvi, Matti Viitanen, Juha O. Rinne, Mikko Hiltunen, Annakaisa Haapasalo, Rashid Giniatullin, Pasi Tavi, Su-Chun Zhang, Katja M. Kanninen, Riikka H. Hämäläinen, Jari Koistinaho in Stem Cell Reports. Published online November 16 2017 doi:10.1016/j.stemcr.2017.10.016

Abstract

PSEN1 Mutant iPSC-Derived Model Reveals Severe Astrocyte Pathology in Alzheimer’s Disease

Highlights

•PSEN1 mutant AD astrocytes manifest hallmarks of AD pathology

•Altered mitochondrial metabolism in AD astrocytes increases oxidative stress

•AD astrocytes reduce the calcium signaling activity of healthy neurons

•Astrocytes are important in the pathogenesis of AD

Summary

Alzheimer’s disease (AD) is a common neurodegenerative disorder and the leading cause of cognitive impairment. Due to insufficient understanding of the disease mechanisms, there are no efficient therapies for AD. Most studies have focused on neuronal cells, but astrocytes have also been suggested to contribute to AD pathology. We describe here the generation of functional astrocytes from induced pluripotent stem cells (iPSCs) derived from AD patients with PSEN1 ΔE9 mutation, as well as healthy and gene-corrected isogenic controls. AD astrocytes manifest hallmarks of disease pathology, including increased β-amyloid production, altered cytokine release, and dysregulated Ca2+ homeostasis. Furthermore, due to altered metabolism, AD astrocytes show increased oxidative stress and reduced lactate secretion, as well as compromised neuronal supportive function, as evidenced by altering Ca2+ transients in healthy neurons. Our results reveal an important role for astrocytes in AD pathology and highlight the strength of iPSC-derived models for brain diseases.

“PSEN1 Mutant iPSC-Derived Model Reveals Severe Astrocyte Pathology in Alzheimer’s Disease” by Minna Oksanen, Andrew J. Petersen, Nikolay Naumenko, Katja Puttonen, Šárka Lehtonen, Max Gubert Olivé, Anastasia Shakirzyanova, Stina Leskelä, Timo Sarajärvi, Matti Viitanen, Juha O. Rinne, Mikko Hiltunen, Annakaisa Haapasalo, Rashid Giniatullin, Pasi Tavi, Su-Chun Zhang, Katja M. Kanninen, Riikka H. Hämäläinen, Jari Koistinaho in Stem Cell Reports. Published online November 16 2017 doi:10.1016/j.stemcr.2017.10.016

http://neurosciencenews.com/alzheimers-astrocytes-7967/

Parkinson's disease: What you need to know in wake of Jesse Jackson's diagnosis

• By MICHAEL CHAN MD
 

Nov 17, 2017

Jesse Jackson

Iconic American civil rights activist, politician and minister Jesse Jackson announced Friday that his doctors have diagnosed him with Parkinson’s disease – a diagnosis that he says comes after several years of symptoms.

Below are answers to some of the more common questions about this disease.

What is Parkinson’s disease?

Parkinson's disease is the second most common neurodegenerative disorder globally, after Alzheimer's disease, affecting more than 1 million people in North America. It was originally described by English surgeon James Parkinson in 1817. While the precise causes of this condition remain unknown, the disease is characterized by abnormalities in a specific region of the brain called the substantia nigra, and it results in decreased signaling of the neurotransmitter dopamine. This imbalance leads to the hallmark symptoms of this condition -- abnormal movements, such as a characteristic hand tremor, slow movements, muscle stiffening, and a decreased ability of the body’s reflexes to appropriately adjust to changes in posture. Psychiatric symptoms often include anxiety and depression. Other characteristic symptoms include walking in short, shuffling steps and decreased facial expressiveness, called “masked facies.”

Who is affected by this condition?

There are an estimated 7.5 million people worldwide living with Parkinson’s, and the risk of developing it increases with age. Approximately 41 per 100,000 persons aged 40 to 49 years has Parkinson's, compared to an estimated 1,900 per 100,000 persons over the age of 79.

What are the risk factors for Parkinson’s?

Aside from older age, the most well-established risk factor for developing Parkinson’s is having a family member who has been diagnosed with this disease, as was the case with Jackson. Men are also 1.5 times more likely to develop Parkinson’s than women. Several large studies have also found a correlation between depression and the development of Parkinson’s, though it is unknown if depression plays a causative role in the development of Parkinson’s, or if it is instead an early symptom. Other possible risk factors include exposure to certain types of pesticides and high consumption of dairy products.

How is Parkinson’s diagnosed?

Parkinson’s is diagnosed based on a patient’s clinical history and physical exam. Diagnosis is made by the when a person has Parkinsonian symptoms without any other explanation, such as another neurological disease, head trauma, or a medication that may also be causing Parkinson’s-like symptoms. There are currently no available laboratory or imaging tests that can confirm a diagnosis of Parkinson’s.

What are the treatments for this condition?

Treatments for Parkinson’s are aimed at correcting the abnormalities in brain dopamine levels and usually include a medication called levodopa or other dopamine-stimulating drugs. These drugs, however, pose a risk of causing uncontrollable movements called dyskinesia. Younger patients with Parkinson’s-associated tremor may benefit from using drugs in a class known as anticholinergics. Some patients who experience symptoms despite medications may benefit from placement of a stimulation device deep in their brains or other neurosurgical procedures. Physical therapy and speech therapy can also be used to help minimize the effects of the disease. Researchers are working on developing gene therapies or methods of neural transplantation to slow or reverse the effects of Parkinson’s, but management with medications and symptomatic support remain the current mainstay of treatment at this time.

What is the prognosis for Parkinson’s?

Neurologic changes seen in Parkinson’s are typically irreversible and may worsen as the disease progresses. The number and severity of symptoms vary from person to person, and there are currently no ways to predict which individuals will experience a rapid or slow decline. Parkinson’s itself is generally not considered to be a fatal disease in and of itself; however, the neurologic changes caused by Parkinson’s increase a person’s likelihood of dying from conditions such as pneumonia due to difficulty swallowing or trauma from falling.

http://abcnews.go.com/Health/parkinsons-disease-wake-jesse-jacksons-diagnosis/story?id=51228890 

Jesse Jackson Reveals He Has Parkinson’s Disease

November 17, 2017   By SOPHIA TAREEN

https://youtu.be/_vN6RvF_Wc0

CHICAGO — The Rev. Jesse Jackson disclosed publicly Friday that he has been seeking outpatient care for two years for Parkinson’s disease and plans to “dedicate” himself to physical therapy.

In a Friday letter to supporters, the 76-year-old civil rights leader said family and friends noticed a change in him about three years ago. He said he could no longer ignore symptoms of the chronic neurological disorder that causes movement difficulties.

“Recognition of the effects of this disease on me has been painful, and I have been slow to grasp the gravity of it,” he wrote. “For me, a Parkinson’s diagnosis is not a stop sign but rather a signal that I must make lifestyle changes and dedicate myself to physical therapy in hopes of slowing the disease’s progression.”

He noted that the same disease “bested my father.” Noah Lewis Robinson Sr. died in 1997 at age 88.

Jackson also released a Northwestern Medicine letter saying he was diagnosed in 2015 and has since sought outpatient care.

He runs the Chicago-based Rainbow/PUSH Coalition and was twice a candidate for the Democratic presidential nomination in the 1980s. He’s remained a strong voice in anti-discrimination efforts, including advocating for affordable housing, and been a fixture at protests nationwide.

He said Friday in the letter that he is also working on a memoir.

“I will continue to try to instill hope in the hopeless, expand our democracy to the disenfranchised and free innocent prisoners around the world,” he said in the letter. “I steadfastly affirm that I would rather wear out than rust out.”

Jackson declined further comment Friday.

http://www.pe.com/2017/11/17/rev-jesse-jackson-discloses-parkinsons-disease-diagnosis/

FDA to crack down on risky stem cell offerings

November 16, 2017by Matthew Perrone

In this Dec. 5, 2014 file photo, a doctor injects a patient with a solution he says is rich in adult stem cells, at his practice in Beverly Hills, Calif. On Thursday, Nov. 16, 2017, the Food and Drug Administration laid out a strategy for regulating cell-based medicine, amid an effort to police a burgeoning medical field that has received little oversight. (AP Photo/Raquel Maria Dillon)

U.S. health authorities announced plans Thursday to crack down on doctors pushing stem cell procedures that pose the gravest risks to patients amid an effort to police a burgeoning medical field that previously has received little oversight.

The Food and Drug Administration laid out a strategy for regulating cell-based medicine, including hundreds of private clinics that have opened across the nation in the last decade. Many of the businesses promote stem cell injections for dozens of diseases including arthritis, multiple sclerosis and even Alzheimer's. They can cost $5,000 to $50,000, but there's little research that such procedures are safe or effective.

Researchers for years have called for a crackdown. FDA officials said they will focus their enforcement efforts on "bad actors" who inject stem cell mixtures into the bloodstream, nervous system or eyes. Regulators say those procedures pose the biggest risk to patients.

"We're going to be prioritizing places where we see products—not just being promoted inappropriately—but putting patients at potential risk," FDA Commissioner Scott Gottlieb told reporters on a conference call.

Gottlieb said the agency plans to use discretion in overseeing lower-risk procedures such as injections for achy joints, adding that this approach would allow the agency to get the "most bang for our regulatory buck." He also said the agency needs to be "nimble and creative" in its regulation to encourage legitimate researchers in the field.

Stem cells have long been recognized for their ability to reproduce and regenerate tissue. And while emerging research suggests that they will eventually be used to treat a range of debilitating diseases, they are currently only approved for a handful of medical procedures. For instance, adult stem cells from bone marrow transplants have long been used to treat leukemia and other blood diseases.

Most of the new clinics offer adults stem cells isolated from fat. Practitioners collect the fluid from patients via liposuction, treat it with chemicals and then inject it back into the body to treat various conditions.

Three Florida women were left nearly or completely blind by one such fat-based procedure, according to a report published earlier this year in the New England Journal of Medicine. The Florida Medical board previously revoked the license of another stem cell practitioner after two patients died under his care after receiving IV drips of stem cells to the bloodstream.

In August the FDA took action against clinics in Florida and California. The agency issued a warning letter to Sunrise, Florida-based US Stem Cell Clinic for marketing unapproved procedures for heart disease, Parkinson's disease and other conditions. And U.S. marshals, under FDA instructions, seized vials of an unproven vaccine from StemImmune Inc. of San Diego.

The FDA's authority to regulate stem cell procedures is a murky area that has been debated for years.

Typically the agency does not regulate individual doctors or their in-office procedures, focusing instead on products developed by drug and medical device manufacturers. But FDA has asserted its authority in certain cases when doctors begin processing stem cells and marketing them to treat serious diseases.

Guidelines released by the agency Thursday aim to clarify how much processing cells can undergo before triggering FDA regulation.

https://medicalxpress.com/news/2017-11-health-agency-risky-stem-cell.html

Stress Can Lead to Risky Decisions

NEUROSCIENCE NEWS   NOVEMBER 16, 2017
Source: MIT.

Summary: Researchers report chronic stress can influence how we make decisions. In a new study, mice who were affected by chronic stress were more likely to make more risky decisions with higher payoff options than those who were less stressed.

MIT neuroscientists have discovered that making decisions, especially when choosing between two options that have both positive and negative elements, can be dramatically affected by chronic stress. NeuroscienceNews.com image is credited to Christine Daniloff/MIT.

Making decisions is not always easy, especially when choosing between two options that have both positive and negative elements, such as deciding between a job with a high salary but long hours, and a lower-paying job that allows for more leisure time.

MIT neuroscientists have now discovered that making decisions in this type of situation, known as a cost-benefit conflict, is dramatically affected by chronic stress. In a study of mice, they found that stressed animals were far likelier to choose high-risk, high-payoff options.

The researchers also found that impairments of a specific brain circuit underlie this abnormal decision making, and they showed that they could restore normal behavior by manipulating this circuit. If a method for tuning this circuit in humans were developed, it could help patients with disorders such as depression, addiction, and anxiety, which often feature poor decision-making.

“One exciting thing is that by doing this very basic science, we found a microcircuit of neurons in the striatum that we could manipulate to reverse the effects of stress on this type of decision making. This to us is extremely promising, but we are aware that so far these experiments are in rats and mice,” says Ann Graybiel, an Institute Professor at MIT and member of the McGovern Institute for Brain Research.

Graybiel is the senior author of the paper, which appears in Cell on Nov. 16. The paper’s lead author is Alexander Friedman, a McGovern Institute research scientist.

Hard decisions

In 2015, Graybiel, Friedman, and their colleagues first identified the brain circuit involved in decision making that involves cost-benefit conflict. The circuit begins in the medial prefrontal cortex, which is responsible for mood control, and extends into clusters of neurons called striosomes, which are located in the striatum, a region associated with habit formation, motivation, and reward reinforcement.

In that study, the researchers trained rodents to run a maze in which they had to choose between one option that included highly concentrated chocolate milk, which they like, along with bright light, which they don’t like, and an option with dimmer light but weaker chocolate milk. By inhibiting the connection between cortical neurons and striosomes, using a technique known as optogenetics, they found that they could transform the rodents’ preference for lower-risk, lower-payoff choices to a preference for bigger payoffs despite their bigger costs.

In the new study, the researchers performed a similar experiment without optogenetic manipulations. Instead, they exposed the rodents to a short period of stress every day for two weeks.

Before experiencing stress, normal rats and mice would choose to run toward the maze arm with dimmer light and weaker chocolate milk about half the time. The researchers gradually increased the concentration of chocolate milk found in the dimmer side, and as they did so, the animals began choosing that side more frequently.

However, when chronically stressed rats and mice were put in the same situation, they continued to choose the bright light/better chocolate milk side even as the chocolate milk concentration greatly increased on the dimmer side. This was the same behavior the researchers saw in rodents that had the prefrontal cortex-striosome circuit disrupted optogenetically.

“The result is that the animal ignores the high cost and chooses the high reward,” Friedman says.

The findings help to explain how stress contributes to substance abuse and may worsen mental disorders, says Amy Arnsten, a professor of neuroscience and psychology at the Yale University School of Medicine, who was not involved in the research.

“Stress is ubiquitous, for both humans and animals, and its effects on brain and behavior are of central importance to the understanding of both normal function and neuropsychiatric disease. It is both pernicious and ironic that chronic stress can lead to impulsive action; in many clinical cases, such as drug addiction, impulsivity is likely to worsen patterns of behavior that produce the stress in the first place, inducing a vicious cycle,” Arnsten wrote in a commentary accompanying the Cell paper, co-authored by Daeyeol Lee and Christopher Pittenger of the Yale University School of Medicine.

Circuit dynamics

The researchers believe that this circuit integrates information about the good and bad aspects of possible choices, helping the brain to produce a decision. Normally, when the circuit is turned on, neurons of the prefrontal cortex activate certain neurons called high-firing interneurons, which then suppress striosome activity.

When the animals are stressed, these circuit dynamics shift and the cortical neurons fire too late to inhibit the striosomes, which then become overexcited. This results in abnormal decision making.

“Somehow this prior exposure to chronic stress controls the integration of good and bad,” Graybiel says. “It’s as though the animals had lost their ability to balance excitation and inhibition in order to settle on reasonable behavior.”

Once this shift occurs, it remains in effect for months, the researchers found. However, they were able to restore normal decision making in the stressed mice by using optogenetics to stimulate the high-firing interneurons, thereby suppressing the striosomes. This suggests that the prefronto-striosome circuit remains intact following chronic stress and could potentially be susceptible to manipulations that would restore normal behavior in human patients whose disorders lead to abnormal decision making.

“This state change could be reversible, and it’s possible in the future that you could target these interneurons and restore the excitation-inhibition balance,” Friedman says.

ABOUT THIS NEUROSCIENCE RESEARCH ARTICLE

Funding: The research was funded by the National Institutes of Health/National Institute for Mental Health, the CHDI Foundation, the Defense Advanced Research Projects Agency and the U.S. Army Research Office, the Bachmann-Strauss Dystonia and Parkinson Foundation, the William N. and Bernice E. Bumpus Foundation, Michael Stiefel, the Saks Kavanaugh Foundation, and John Wasserlein and Lucille Braun.

Source: Anne Trafton – MIT

Publisher: Organized by NeuroscienceNews.com.

Image Source: NeuroscienceNews.com image is credited to Christine Daniloff/MIT.

Original Research: The study will appear in Cell.

http://neurosciencenews.com/stress-risky-decisions-7960/