TRANSLATE

Welcome to Our Parkinson's Place


I copy news articles pertaining to research, news and information for Parkinson's disease, Dementia, the Brain, Depression and Parkinson's with Dystonia. I also post about Fundraising for Parkinson's disease and events. I try to be up-to-date as possible. I have Parkinson's
diseases as well and thought it would be nice to have a place where
updated news is in one place. That is why I began this blog.
I am not responsible for it's contents, I am just a copier of information searched on the computer. Please understand the copies are just that, copies and at times, I am unable to enlarge the wording or keep it uniformed as I wish. This is for you to read and to always keep an open mind.
Please discuss this with your doctor, should you have any questions, or concerns. Never do anything without talking to your doctor. I do not make any money from this website. I volunteer my time to help all of us to be informed. Please no advertisers. This is a free site for all.
Thank you.


Saturday, November 19, 2016

Lewy body dementia may often be misdiagnosed as Alzheimer’s disease: Study

By: Dr. Victor Marchione | Brain Function | Saturday, November 19, 2016 



Lewy body dementia (LBD) may often be misdiagnosed as Alzheimer’s disease, according to research findings. Howard I. Hurtig, chair at the department of neurology, Pennsylvania Hospital warned, “While the symptoms of LBD may be similar to Alzheimer’s and Parkinson’s disease, the treatment strategy is more challenging because fewer medications can be used safely. I cannot overemphasize the need to avoid medications that can worsen the symptoms of LBD. Every patient with this disease and their caregivers should be familiar with the list of acceptable and forbidden drugs.”
According to the National Institute of Neurological Disorders and Stroke, what’s called Lewy body dementia has three distinguishing features that eventually become apparent:Fluctuating alertness and attention resembling deliriumvisual hallucinations, and Parkinson’s-like symptoms, like tremors, rigidity, and even balance problems.
It’s this mixture of symptoms – not to mention LBD’s similarity to diseases like Alzheimer’s and Parkinson’s – that makes it difficult to diagnosis. What’s more, LBD patients can easily have a bad day whenever they are poorly responsive, not knowing what time it is or where they are. But then the next day, they are their normal self once more, able to discuss their favorite TV show and distant memories equally.
As a result, it can be pretty disabling for LBD patients and upsetting for family members and caregivers alike.

What is Lewy body dementia exactly?

While looking at Parkinson’s disease in the early 1900s, scientist Friederich H. Lewy discovered abnormal protein deposits that disrupt the brain’s normal functioning. These Lewy body proteins are found in an area of the brain stem – basically, where they deplete the neurotransmitter dopamine, causing Parkinson’s-like symptoms.
In LBD, these abnormal proteins are spread throughout other areas of the brain. The brain chemical acetylcholine is then depleted, which adversely affects perception, thinking, and overall behavior. LBD exists on its own or in conjunction with Alzheimer’s disease and Parkinson’s disease.
According to the Lewy Body Dementia Association, LBD is not a rare disease. It affects roughly 1.3 million Americans. LBD now refers to both Parkinson’s disease dementia and dementia with Lewy bodies. The earliest symptoms of these two diseases differ, but are the result of the same biological changes in the brain. Over a period of time, people with both diagnoses will develop similar cognitive, physical, sleep, and behavioral symptoms.
Although the cause of LBD isn’t exactly clear, several factors may increase the risk of developing the disease – such as being male and older than 60, as well as having a family member with LBD.
On average, the disease has a duration of five to seven years. But it can still continue anywhere between two and 20 years, depending on a person’s overall health, age, and severity of symptoms.

Treatment options for Lewy body dementia

There’s no cure for LBD, and treatment can be challenging because each person with LBD and other dementias experiences symptoms differently. Still, the individual symptoms of LBD can be treated by patients and caregivers, according to the Mayo Clinic.
For one thing, Alzheimer’s disease medications like rivastigmine (Exelon) help increase the levels of chemical messengers (neurotransmitters) thought to be important for memory, thought, and judgment in the brain. This can improve alertness and cognition, and may help reduce hallucinations and other behavioral problems. Possible side effects may include gastrointestinal upset, excessive salivation and tearing, and frequent urination.
Sometimes, simply modifying a patient’s environment helps. That’s because reducing clutter and distracting noise can make it easier for someone with dementia to focus. It can also reduce the risk of hallucinations in people with LBD.
We all know that exercise benefits everyone, including people with dementia. Exercising may slow the progression of impaired thinking in LBD patients. Crossword puzzles and other thinking activities may be beneficial, too.

In order to help prevent nighttime restlessness and disorientation, patients and caregivers should try limiting caffeine during the day, eliminating daytime napping, and establishing a sound nighttime ritual.
Alternatively, you can try medicine and techniques that help promote relaxation, too: Music therapy, which involves listening to soothing music; pet therapy, which involves visits from animals to promote improved moods and behaviors in people with dementia; aromatherapy, which uses fragrant plant oils; and finally, massage therapy.
It’s important to note that it may take more than a year or two for enough LBD symptoms to develop. That’s why it’s critical to pursue a formal diagnosis and treatment early on. It will make a difference to quality of life.
http://www.belmarrahealth.com/lewy-body-dementia-may-often-misdiagnosed-alzheimers-disease-study/

3-D Imaging Technique Maps Migration of DNA-Carrying Material at the Center of Cells

NEUROSCIENCE NEWS  NOVEMBER 17, 2016

Summary: Researchers have mapped the reorganization of genetic material that takes place when a stem cell matures into a nerve cell.


Source: DOE/Lawrence Berkeley National Laboratory.

This computer rendering shows the skeletonized structure of heterochromatin (red represents a thin region while white represents a thick region), a tightly packed form of DNA, surrounding another form of DNA-carrying material known as euchromatin (dark blue represents a thin region and yellow represent the thickest) in a mouse’s mature nerve cell. NeuroscienceNews.com image is credited to Berkeley Lab, UCSF.

X-ray technique at Berkeley Lab provides high-res views of the structure and movement of genetic material in cell nuclei.

Scientists have mapped the reorganization of genetic material that takes place when a stem cell matures into a nerve cell. Detailed 3-D visualizations show an unexpected connectivity in the genetic material in a cell’s nucleus, and provide a new understanding of a cell’s evolving architecture.

These unique 3-D reconstructions of mouse olfactory cells, which govern the sense of smell, were obtained using X-ray imaging tools at the Department of Energy’s Lawrence Berkeley National Laboratory (Berkeley Lab). The results could help us understand how patterning and reorganization of DNA-containing material called chromatin in a cell’s nucleus relate to a cell’s specialized function as specific genes are activated or silenced.
Chromatin is compacted to form chromosomes, which pass along an organism’s genetic fingerprint to newly formed cells during cell division.

The results were published this week in a special edition of Cell Reports that highlights epigenetics, a field of study focused on a layer of biochemistry that affects gene expression and that is closely coupled to DNA but does not alter the genetic code.
Researchers used a powerful X-ray microscope at Berkeley Lab’s Advanced Light Source (ALS) to capture images of nerve cell samples at different stages of maturity as they became more specialized in their function — this process is known as “differentiation.” Cells at each stage were imaged from dozens of different angles using X-rays. Each set of 2-D images was used to calculate a 3-D reconstruction of a cell detailing the changing chromatin formations in the nuclei.

They also were able to measure the dense packing in a form of chromatin called heterochromatin, and they learned about the importance of a specific protein in controlling the compaction of heterochromatin and its confinement to the nucleus.

“It’s a new way of looking at the nucleus where we don’t have to chemically treat the cell,” said Carolyn Larabell, director of the National Center for X-ray Tomography (NCXT), a joint program of Berkeley Lab and UC San Francisco (UCSF). “Being able to directly image and quantify changes in the nucleus is enormously important and has been on cell biologists’ wish list for many years.”

Chromatin is “notoriously sensitive,” she said, to chemical stains and other chemical additives that are often used in biological imaging to highlight regions of interest in a given sample. “Until now, it has only been possible to image the nucleus indirectly by staining it, in which case the researcher has to take a leap of faith that the stain was evenly distributed.”

Larabell, a faculty scientist at Berkeley Lab and a UCSF professor, said it was previously thought that chromatin existed as a series of disconnected islands, though the latest study showed how the chromatin is compartmentalized into two distinct regions of “crowding” that form a continuous network throughout the nucleus.

“We were really surprised: There are no islands, it’s all connected,” she said, adding, “We could see how chromatins pack through the nucleus and how molecules move through the nucleus, and we found that heterochromatin is 30 percent more crowded than the region where active genes are. That cannot be done with any other imaging techniques.” Two-dimensional images would have shown the nucleus as a “flat, confusing mess,” she said.
One aim of the latest study was to gain new insight into gene expression in mice specific to olfactory genes. Mice have about 1,500 genes related to smell. Each olfactory nerve cell expresses just one of these olfactory genes to produce a receptor that recognizes a related set of odors. The many receptors in a mouse’s nasal cavity allow it to detect a wide range of smells.

These renderings show a tightly packed form of DNA called heterochromatin, as it exists in a mouse cell’s nucleus, at different stages of cell development: a multipotent stem cell (left), a neuronal progenitor (middle), and a mature nerve cell (right). Credit: Berkeley Lab, UCSF.


“We’re trying to understand how the reorganization of chromatin affects gene expression,” Larabell said. “No one’s been able to study this at the human level yet.” This research will hopefully lead to new insights about diseases and disorders that relate to gene expression. Already, the study’s results are being incorporated into models of cell development.
One of the precursors to Alzheimer’s disease, which attacks the brain’s nerve cells, is a loss of smell, so understanding this connection to olfactory nerve cells could perhaps serve as a diagnostic tool and perhaps unlock a deeper understanding of the degenerative disorder.

The latest study used a microscopy technique known as soft X-ray tomography to record a series of images from small groups of dozens of frozen olfactory nerve cells in three separate stages of development. The technique, which is unique to Berkeley Lab’s ALS, captured details as small as tens of nanometers, or tens of billionths of a meter. Researchers visually distinguished regions of highly compacted heterochromatin from other chromatin types.




This animation shows a 3-D rendering of a nucleus in a mouse cell known as a “neuronal progenitor.” The view shown here slices from the surface of the nucleus through to its other side, and is color-coded for two types of genetic material: heterochromatin (blue) and euchromatin (green). The gold color represents mitochondria, the energy production center in cells. Heterochromatin is believed to be the most tightly packed form of chromatin. Neuronal progenitor cells resemble stem cells in that they have the ability to specialize into different cell types, though with a more limited range of differentiation. (Credit: Berkeley Lab, UCSF)

With the proven success of the imaging technique, Larabell said it’s possible to perform statistical analyses based on large collections of cell nuclei images sorted by different stages of development. Coupled with other types of imaging techniques, researchers hope to isolate individual gene-selection processes in upcoming work.

“This work highlights the power of multidisciplinary research,” said Mark Le Gros, associate director of the NCXT and a physicist who was responsible for the design and construction of the X-ray microscope. Le Gros, the lead author in this research, added, “This is an example of work that required a combination of molecular biologists and cell biologists with physicists and computer scientists.”
ABOUT THIS GENETICS RESEARCH ARTICLE
The Advanced Light Source is a DOE Office of Science User Facility.
The latest work also featured participation from researchers at the Foundation for Research and Technology-Hellas in Greece, Massachusetts Institute of Technology, and University of Jyväskylä in Finland. 
Funding: The work was supported by the National Institutes of Health.
Source: Glenn Roberts Jr – DOE/Lawrence Berkeley National Laboratory 
Image Source: NeuroscienceNews.com image is credited to Berkeley Lab, UCSF.
Video Source: The video is credited to Berkeley Lab.
Original Research: Full open access research for “Soft X-Ray Tomography Reveals Gradual Chromatin Compaction and Reorganization during Neurogenesis In Vivo” by Mark A. Le Gros, E. Josephine Clowney, Angeliki Magklara, Angela Yen, Eirene Markenscoff-Papadimitriou, Bradley Colquitt, Markko Myllys, Manolis Kellis, Stavros Lomvardas, and Carolyn A. Larabell in Cell Reports. Published online November 15 2016 doi:10.1016/j.celrep.2016.10.060


Abstract

Soft X-Ray Tomography Reveals Gradual Chromatin Compaction and Reorganization during Neurogenesis In Vivo
Highlights
•Soft X-ray tomography reveals chromatin networks in olfactory neurons
•Chromatin compaction increases during olfactory neurogenesis
•Condensed chromatin moves to nuclear core during differentiation
•HP1β regulates reorganization of chromatin in mature neurons

Summary
The realization that nuclear distribution of DNA, RNA, and proteins differs between cell types and developmental stages suggests that nuclear organization serves regulatory functions. Understanding the logic of nuclear architecture and how it contributes to differentiation and cell fate commitment remains challenging. Here, we use soft X-ray tomography (SXT) to image chromatin organization, distribution, and biophysical properties during neurogenesis in vivo. Our analyses reveal that chromatin with similar biophysical properties forms an elaborate connected network throughout the entire nucleus. Although this interconnectivity is present in every developmental stage, differentiation proceeds with concomitant increase in chromatin compaction and re-distribution of condensed chromatin toward the nuclear core. HP1β, but not nucleosome spacing or phasing, regulates chromatin rearrangements because it governs both the compaction of chromatin and its interactions with the nuclear envelope. Our experiments introduce SXT as a powerful imaging technology for nuclear architecture.

“Soft X-Ray Tomography Reveals Gradual Chromatin Compaction and Reorganization during Neurogenesis In Vivo” by Mark A. Le Gros, E. Josephine Clowney, Angeliki Magklara, Angela Yen, Eirene Markenscoff-Papadimitriou, Bradley Colquitt, Markko Myllys, Manolis Kellis, Stavros Lomvardas, and Carolyn A. Larabell in Cell Reports. Published online November 15 2016 doi:10.1016/j.celrep.2016.10.060

http://neurosciencenews.com/3d-imaging-genetics-cells-5545/

New Insight Into How Alzheimer’s Begins

NEUROSCIENCE NEWS
Summary: Researchers discover a way doctors can detect early signs of Alzheimer’s by looking at the back of patients’ eyes.


Source: UTMB.

UTMB researchers have previously found evidence that a toxic form of tau protein may underlie the early stages of Alzheimer’s.
NeuroscienceNews.com image is adapted from the UTMB press release.



A new study from The University of Texas Medical Branch at Galveston offers important insight into how Alzheimer’s disease begins within the brain. The researchers found a relationship between inflammation, a toxic protein and the onset of the disease. The study also identified a way that doctors can detect early signs of Alzheimer’s by looking at the back of patients’ eyes.

“Early detection of Alzheimer’s warning signs would allow for early intervention and prevention of neurodegeneration before major brain cell loss and cognitive decline occurs,” said lead author Ashley Nilson, a neuroscience graduate student. “Using the retina for detecting AD and other neurodegenerative diseases would be non-invasive, inexpensive and could become a part of a normal screening done at patient checkups.”

UTMB researchers have previously found evidence that a toxic form of tau protein may underlie the early stages of Alzheimer’s. Brain cells depend on tau protein to form highways for the cell to receive nutrients and get rid of waste. In some neurodegenerative diseases like Alzheimer’s, the tau protein changes into a toxic form called tau oligomers and begins clumping into neurofibrillary tangles. When this happens, molecular nutrients can no longer move to where they are needed and the oligomers produce toxic effects leading to the eventual death of the brain cells.

It’s becoming increasingly clear that inflammation within the brain plays an important role in Alzheimer’s development and progression. Inflammation and loss of connections between nerves within the brain happen before the formation of the tangles that are characteristic of this disease. It’s possible that the tau oligomers may be responsible for this inflammation.
In a recent paper in the Journal of Alzheimer’s Disease, UTMB’s research team detailed their investigation on the relationship between inflammation, toxic tau and Alzheimer’s onset by performing systematic analyses of brain and retina samples from people with Alzheimer’s and a mouse model of Alzheimer’s.

The results demonstrated that the toxic tau may induce inflammation in Alzheimer’s. The toxic tau spreads between connected brain regions, which may initiate inflammation in these new regions. This situation can create a cycle of toxic tau, inflammation and cell death throughout the brain over time.

Beyond determining eye health and corrective lens prescriptions, having an eye exam can alert health care professionals of several different health conditions including diabetic complications, high cholesterol and high blood pressure. Now, UTMB researchers found that retina tissue that they studied can show evidence of toxic tau and inflammation.

“Our findings suggest that the degeneration of nerve cells due to chronic inflammation induced by the tau oligomers may be combated through the combination of anti-tau oligomer and anti-inflammatory therapeutics for the treatment of Alzheimer’s and related diseases,” said senior author Rakez Kayed, associate professor in the UTMB Department of Neurology. “Our is continuing to expand our understanding of neurodegenerative diseases.”
ABOUT THIS ALZHEIMER’S DISEASE RESEARCH ARTICLE
The authors include a team of collaborative scientists and doctors including UTMB’s Kelsey English, Julia Gerson, T. Barton Whittle, C. Nicholas Crain, Judy Xue, Urmi Sengupta, Diana Castillo-Carranza, Wenbo Zhang and Praveena Gupta.
Funding: The work was supported by the UTMB Mitchell Center for Neurodegenerative Disease, the University of Texas System Neuroscience and Neurotechnology Research Institute and Retina Foundation and the National Institutes of Health.
Source: Donna Ramirez – UTMB
Image Source: NeuroscienceNews.com image is adapted from the UTMB press release.
Original Research: Full open access research for “Tau Oligomers Associate with Inflammation in the Brain and Retina of Tauopathy Mice and in Neurodegenerative Diseases” byNilson, Ashley N.; English, Kelsey C.; Gerson, Julia E.; Whittle, T. Barton; Crain, C. Nicolas; Xue, Judy; Sengupta, Urmi; Castillo-Carranza, Diana L.; Zhang, Wenbo; Gupta, Praveena; and Kayed, Rakez in Journal of Alzheimer’s Disease. Published online September 12 2016 doi:10.3233/JAD-160912

Abstract

Tau Oligomers Associate with Inflammation in the Brain and Retina of Tauopathy Mice and in Neurodegenerative Diseases

It is well-established that inflammation plays an important role in Alzheimer’s disease (AD) and frontotemporal lobar dementia (FTLD). Inflammation and synapse loss occur in disease prior to the formation of larger aggregates, but the contribution of tau to inflammation has not yet been thoroughly investigated. Tau pathologically aggregates to form large fibrillar structures known as tangles. However, evidence suggests that smaller soluble aggregates, called oligomers, are the most toxic species and form prior to tangles. Furthermore, tau oligomers can spread to neighboring cells and between anatomically connected brain regions. In addition, recent evidence suggests that inspecting the retina may be a window to brain pathology. We hypothesized that there is a relationship between tau oligomers and inflammation, which are hallmarks of early disease. We conducted immunofluorescence and biochemical analyses on tauopathy mice, FTLD, and AD subjects. We showed that oligomers co-localize with astrocytes, microglia, and HMGB1, a pro-inflammatory cytokine. Additionally, we show that tau oligomers are present in the retina and are associated with inflammatory cells suggesting that the retina may be a valid non-invasive biomarker for brain pathology. These results suggest that there may be a toxic relationship between tau oligomers and inflammation. Therefore, the ability of tau oligomers to spread may initiate a feed-forward cycle in which tau oligomers induce inflammation, leading to neuronal damage, and thus more inflammation. Further mechanistic studies are warranted in order to understand this relationship, which may have critical implications for improving the treatment of tauopathies.
“Tau Oligomers Associate with Inflammation in the Brain and Retina of Tauopathy Mice and in Neurodegenerative Diseases” byNilson, Ashley N.; English, Kelsey C.; Gerson, Julia E.; Whittle, T. Barton; Crain, C. Nicolas; Xue, Judy; Sengupta, Urmi; Castillo-Carranza, Diana L.; Zhang, Wenbo; Gupta, Praveena; and Kayed, Rakez in Journal of Alzheimer’s Disease. Published online September 12 2016 doi:10.3233/JAD-160912

http://neurosciencenews.com/alzheimers-tau-progression-5554/

Friday, November 18, 2016

News from the American Neurological Association Annual Meeting: Deep Brain Stimulation Results Encouraging After Five Years of Follow up, Study Finds

Neurology Today:

17 November 2016 - Volume 16 - Issue 22 - p 48–49


ARTICLE IN BRIEF

Patients with early-stage Parkinson's disease who received deep brain stimulation continued to have better motor scores five years later than those who only received medical treatment.

Dr. Mallory Hacker



BALTIMORE — Patients with early-stage Parkinson's disease (PD) who received deep brain stimulation (DBS) continued to have better motor scores five years later than those who only received medical treatment, according to new pilot-study data reported by Vanderbilt University investigators here in October at the annual meeting of the American Neurological Association.

The researchers said the evidence supports the need for a larger phase 3 trial of DBS in patients with very early disease. The FDA has approved such a trial, planned for 280 patients enrolled across 18 US centers, for which researchers are now pursuing funding.
Subthalamic nucleus DBS is already approved for patients with mid- and advanced stage PD, but its efficacy in early PD is still being investigated. Medical therapy is better at controlling symptoms in early PD than in later stages. Other researchers have tried to demonstrate a disease-modifying effect, but no therapy has been definitively shown to halt or slow the progression of disease.

In this study, patients were eligible if they had a stable response to dopaminergic therapy and had been on levodopa or dopamine-agonist therapy for six months to four years. The average duration for medication use before enrollment was just over two years
What's distinct about this population is that these are very early stage Parkinson's disease patients,” said Mallory Hacker, PhD, assistant professor of neurology at Vanderbilt. “Patients couldn't have any signs or history of dyskinesias or motor fluctuations when they enrolled.”

STUDY METHODOLOGY
Thirty patients were randomized to receive either optimal drug therapy alone or deep-brain stimulation plus optimal drug therapy. In this study, DBS therapy was applied to the bilateral subthalamaic nucleus to deliver electrical stimulation to modify the brain circuits responsible for Parkinson's disease symptoms.

After the initial study period of two years, four out of 14 total patients in the optimal drug therapy group elected to receive DBS. Feedback received during peer review also led investigators to narrow the inclusion criteria for medication duration for the future pivotal trial to one to four years.

Patients who had DBS and optimal drug therapy — who had been on medical therapy for one to four years — experienced improvements in motor scores on the United Parkinson's Disease Rating Scale Part III that were an average of 8.9 points better than the group that only received medical therapy five years after baseline (p<.03). That represented more than three times the minimal clinically meaningful change for this measure, researchers noted.
“In this study, the medication group progressively worsens over five years as you would expect in early stage Parkinson's,” Dr. Hacker said. “And these results show that average scores were improved over years for the DBS and optimal drug therapy group.”

Patients on medical therapy for six months to four years at the beginning of the study also showed a trend of greater improvement in motor scores; the DBS and optimal drug therapy group improved by an average of 4.6 points more than the group on medical therapy alone — but the difference wasn't statistically significant.

Dr. Hacker acknowledged the small study size of the pilot trial, but said the results reinforce the rationale for studying DBS further to determine whether the DBS should be offered for patients with very early stage PD.
“This is further evidence to support why a multicenter, pivotal study should be done,” she said.

David Charles, MD, FAAN, professor and vice chairman of neurology, chief medical officer of the Vanderbilt Neuroscience Institute and principal investigator of the study, said: “Our team's overarching goal is to determine if very early DBS will dramatically slow the progression of Parkinson's disease. If that were proven true, it would be a landmark achievement in the battle against this devastating disease.”

EXPERTS COMMENT

Dr. Charles Adler


Charles H. Adler, MD, PhD, FAAN, professor of neurology at the Mayo Clinic in Phoenix, AZ, who conducts research on Parkinson's, said: “This is a very small study so the results need to be interpreted with great caution. But the fact that there were statistically significant differences between these groups is promising.”

Commenting on the abstract, he said he would like to know what medications the patients were taking, and how many of the patients in each group developed motor fluctuations or dyskinesias. As this therapy moves to phase 3, there will be more questions that need to be answered, he said.

“I would like to know more than just the effect on motor score,” he said. “It will be important to know how early DBS might affect activities of daily living, non-motor symptoms, development of motor fluctuations or dyskinesias, overall medication needs, quality of life, etc.”

http://journals.lww.com/neurotodayonline/Fulltext/2016/11170/News_from_the_American_Neurological_Association.14.aspx