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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.


Friday, July 21, 2017

21 Tips for Washing, Grooming and Going to the Bathroom With Parkinson’s Disease

BY WENDY HENDERSON IN SOCIAL CLIPS.
July 20, 2017



As a person’s Parkinson’s disease progresses, simple everyday tasks such as washing, grooming and going to the bathroom can become difficult due to typical Parkinson’s symptoms such as tremors or rigidity. Those living with the disease will be keen to do as much for themselves as possible and retain as much of their independence as they can, particularly when it comes to personal hygiene.
We’ve put together a list of handy tips to help people living with Parkinson’s continue to wash, groom and go to the bathroom easily and safely using information from the National Parkinsons Foundation.
Washing
  • Installing at least two fitted handrails near the bath or shower will allow the patient to grab hold of something safe and secure while getting in and out of the bath or shower. These should be professionally fitted if possible to ensure they are strong enough to support the patient’s weight.
  • A chair or bench in the shower or bathtub will help those who have trouble balancing while standing. A handheld showerhead is best used in these circumstances.
  • Make sure the water isn’t too hot, it should be less than 120ºC.
  • Place non-slip rubber mats in the bath tub and shower cubicle.
  • Bath rugs and mats should have a rubber backing so they don’t slide across tiles.
  • Liquid soap in a pump dispenser is safer to use than hard bars of soap which can slip out of hands and leave slippery residue underfoot.
  • Install a shelf in the shower or bath area that is between knee and shoulder height for easy access to soap, shampoo, and other essential washing items.
  • Advise the patient to always take their cell phone or medical alert device into the bathroom if they’re home alone.
Grooming
  • Patients should sit down when brushing their teeth, shaving, applying makeup or drying their hair so they don’t have to worry about balance.
  • It’s important to support the upper body by resting elbows on the sink or vanity when grooming.
  • Electric devices are often better and safer to use than non-electric ones, such as toothbrushes and shavers.
  • Hands-free hair dryers can be mounted on a vanity unit.
Going to the bathroom and incontinence
  • Toilet frames or grab bars will help patients get up off the toilet safely.
  • Introduce a regular schedule for visiting the bathroom, such as every two hours or before meals.
  • Avoid drinking caffeinated drinks which may cause more frequent bathroom visits.
  • Try to avoid fluids two hours before bed.
  • Patients should use a nightlight or keep the bathroom light on during the night so they can make their way to the bathroom safely.
  • It’s advised that those with Parkinson’s attempt to fully empty their bladder each time they visit the bathroom.
  • If patients become prone to bathroom accidents, they should try using incontinence products such as pads or padded underwear.
  • Patients should seek medical advice if they experience burning or a sudden increase in frequency or urgency to urinate as this may indicate a urinary tract infection.
  • A urologist can help if patients are experiencing problems with incontinence.
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Parkinsons’s News Today is strictly a news and information website about the disease. It does not provide medical advice, diagnosis or treatment. This content is not intended to be a substitute for professional medical advice, diagnosis, or treatment. Always seek the advice of your physician or another qualified health provider with any questions you may have regarding a medical condition. Never disregard professional medical advice or delay in seeking it because of something you have read on this website.

https://parkinsonsnewstoday.com/2017/07/20/tips-washing-grooming-going-bathroom-parkinsons-disease/

Wednesday, July 19, 2017

Why Some Women Are More Likely to Feel Depressed

NEUROSCIENCE NEWS  JULY 19, 2017

Summary: A new study published in the journal Menopause finds longer duration of estrogen exposure from the start of menstruation until the onset of menopause is associated with a reduced risk of depression in women.

Source: NAMS.

A key finding of this study was that longer duration of estrogen exposure from the start of menstruation until the onset of menopause was significantly associated with a reduced risk of depression during the transition to menopause and for up to 10 years postmenopause. NeuroscienceNews.com image is for illustrative purposes only.


New study links duration of estrogen exposure with increased vulnerability to depression: Longer exposure to estrogen shown to provide protection.

It’s no secret that the risk of depression increases for women when their hormones are fluctuating. Especially vulnerable times include the menopause transition and onset of postmenopause. There’s also postpartum depression that can erupt shortly after childbirth. But why do some women feel blue while others seem to skate through these transitions? One answer is provided through study results being published online today in Menopause, the journal of The North American Menopause Society (NAMS).

The article “Lifelong estradiol exposure and risk of depressive symptoms during the transition to menopause and postmenopause” includes data from a study of more than 1,300 regularly menstruating premenopausal women aged 42 to 52 years at study entry. The primary goal of the study was to understand why some women are more vulnerable to depression, even though all women experience hormone fluctuations.

Previous studies have suggested a role for reproductive hormones in causing an increased susceptibility to depression. This study focused largely on the effect of estradiol, the predominant estrogen present during the reproductive years. Among other things, estradiol modulates the synthesis, availability, and metabolism of serotonin, a key neurotransmitter in depression. Whereas fluctuations of estradiol during the menopause transition are universal, the duration of exposure to estradiol throughout the adult years varies widely among women.

A key finding of this study was that longer duration of estrogen exposure from the start of menstruation until the onset of menopause was significantly associated with a reduced risk of depression during the transition to menopause and for up to 10 years postmenopause. Also noteworthy was that longer duration of birth control use was associated with a decreased risk of depression, but the number of pregnancies or incidence of breastfeeding had no association.

“Women are more vulnerable to depressive symptoms during and after the menopause transition because of fluctuating hormone changes,” says Dr. JoAnn Pinkerton, executive director of NAMS. “This study additionally found a higher risk for depression in those with earlier menopause, fewer menstrual cycles over lifespan, or more frequent hot flashes. Women and their providers need to recognize symptoms of depression such as mood changes, loss of pleasure, changes in weight or sleep, fatigue, feeling worthless, being unable to make decisions, or feeling persistently sad and take appropriate action.”
ABOUT THIS NEUROSCIENCE RESEARCH ARTICLE
Source: Eileen Petridis – NAMS
Image Source: NeuroscienceNews.com image is in the public domain.
Original Research: The study will appear in Menopause.

http://neurosciencenews.com/women-estrogen-depression-7122/

Steering an Enzyme’s ‘Scissors’ Shows Potential for Stopping Alzheimer’s

NEUROSCIENCE NEWS        JULY 19, 2017

Summary: Researchers at UBC believe they have identified a method that could help stop Alzheimer’s disease in its tracks.

Source: UBC.


How one amino acid can spell the difference between a healthy aging brain and early onset Alzheimer’s disease. NeuroscienceNews.com image is credited to Brian Kladko and Weihong Song/University of British Columbia.


How one amino acid can spell difference between a healthy aging brain and early onset Alzheimer’s disease.

The old real estate adage about “location, location, location” might also apply to the biochemical genesis of Alzheimer’s disease, according to new research from the University of British Columbia.

Scientists had previously identified a couple of crucial steps in the formation of a protein called amyloid beta, which accumulates in clumps, or “plaques,” in the brains of people with Alzheimer’s disease. Those discoveries inspired efforts at disrupting the biochemical carving of amyloid beta’s precursor protein into its final, toxic shape.

The latest drugs being tested try to silence an enzyme, called BACE1, that cuts the precursor protein. But BACE1 has other functions that are beneficial, so stopping it altogether could bring unwanted side effects — including disrupting the production of myelin, the protective insulation of brain cells.

Psychiatry Professor and Alzheimer’s researcher Weihong Song has found that changing where the cut is made — in effect, guiding the enzyme’s scissors to a different point — could achieve the same goal, with less collateral damage.

Song built upon two discoveries in the past decade of two rare mutations: one found in Italian people that leads to early onset Alzheimer’s disease, and another found in Icelandic people that staves off Alzheimer’s disease.

Dr. Song’s team at UBC’s Townsend Family Laboratories was particularly intrigued by the diametrically opposite effects of both mutations because they affected the same point on the precursor protein’s chain of 770 amino acids, swapping one acid for another.

As Dr. Song and his team describe in the July 19 issue of the Journal of Neuroscience, they injected one set of mice with a virus carrying the Italian gene mutation, and another set with the Icelandic mutation.

They found that the amino acid substitution affected where the precursor protein was cleaved. The Icelandic mutation resulted in a shortened form of amyloid beta, which does not become “sticky” and turn into plaque. The Italian mutation produced a longer, “stickier” version of amyloid beta, which ultimately becomes neuron-smothering plaque.

Actually, the effects were a matter of degree: Each mutation led to more cuts in one location or more cuts in the other location. But in the gradual degradation of Alzheimer’s disease, that could be enough – reducing the levels of the offending toxin could translate into many more years of life before cognitive decline sets in.

“If we can adjust where BACE1 cuts the precursor protein, we will have a very precise way of slowing the build-up of plaque in the brain, without affecting other processes,” says Dr. Song, a Canada Research Chair in Alzheimer’s Disease and the Jack Brown and Family Professor. “This provides a new target in our search for a drug – instead of sledgehammer, it’s more like a scalpel.”
ABOUT THIS NEUROSCIENCE RESEARCH ARTICLE
Funding: This research was supported by Canadian Institutes of Health Research, Alzheimer’s Society of Canada, University of British Columbia.
Source: Brian Kladko – UBC
Image Source: NeuroscienceNews.com image is credited to Brian Kladko and Weihong Song/University of British Columbia.

Original Research: Abstract for “BACE1 Cleavage Site Selection Critical for Amyloidogenesis and Alzheimer’s Pathogenesis” by Shuting Zhang, Zhe Wang, Fang Cai, Mingming Zhang, Yili Wu, Jing Zhang and Weihong Song in Journal of Neuroscience. Published online July 19 2017 doi:10.1523/JNEUROSCI.0340-17.2017

Abstract

BACE1 Cleavage Site Selection Critical for Amyloidogenesis and Alzheimer’s Pathogenesis

Mutations in amyloid β precursor protein (APP) gene alter APP processing, either causing familial Alzheimer’s disease (AD) or protecting against dementia. Under normal conditions, β-site APP cleaving enzyme 1 (BACE1) cleaves APP at minor Asp1 site to generate C99 for amyloid β protein (Aβ) production, and predominantly at major Glu11 site to generate C89, resulting in truncated Aβ production. We discovered that A673V mutation, the only recessive AD-associated APP mutation, shifted the preferential β-cleavage site of BACE1 in APP from the Glu11 site to the Asp1 site both in male and female transgenic mice in vivo and in cell lines and primary neuronal culture derived from timed pregnant rats in vitro, resulting in a much higher C99 level and C99/C89 ratio. All other mutations at this site, including the protective Icelandic A673T mutation, reduced C99 generation, and decreased the C99/C89 ratio. Furthermore, A673V mutation caused stronger dimerization between mutant and wild-type APP, enhanced the lysosomal degradation of the mutant APP, and inhibited γ-secretase cleavage of the mutant C99 to generate Aβ, leading to recessively inherited AD. The results demonstrate that APP673 regulates APP processing and the BACE1 cleavage site selection is critical for amyloidogenesis in AD pathogenesis, and implicate a pharmaceutical potential for targeting the APP673 site for AD drug development.



SIGNIFICANCE STATEMENT β-site APP cleaving enzyme 1 (BACE1) is essential for amyloid β protein production. We discovered that A673V mutation shifted the BACE1 cleavage site from the Glu11 to the Asp1 site, resulting in much higher C99 level and C99/C89 ratio. All other mutations at this site of amyloid β precursor protein (APP) reduced C99 generation and decreased the C99/C89 ratio. Furthermore, A673V mutation resulted in stronger dimerization between mutant and wild-type APP, enhanced the lysosomal degradation of the mutant APP, and inhibited γ-secretase cleavage of the mutant C99 to generate amyloid β protein, leading to recessively inherited Alzheimer’s disease (AD). The results demonstrate that APP673 regulates APP processing, and the BACE1 cleavage site selection is critical for amyloidogenesis in AD pathogenesis, and implicate a pharmaceutical potential for targeting the APP673 site for AD drug development.
“BACE1 Cleavage Site Selection Critical for Amyloidogenesis and Alzheimer’s Pathogenesis” by Shuting Zhang, Zhe Wang, Fang Cai, Mingming Zhang, Yili Wu, Jing Zhang and Weihong Song in Journal of Neuroscience. Published online July 19 2017 doi:10.1523/JNEUROSCI.0340-17.201

http://neurosciencenews.com/enzyme-stop-alzheimers-7129/

Blood Test Identifies Key Alzheimer’s Marker

NEUROSCIENCE NEWS   JULY 19, 2017


Summary: Researchers have devised a new blood test that can detect if amyloid had begun to accumulate in the brain. The test help physicians diagnose Alzheimer’s disease in a cheaper, less invasive way than currently available. The researchers will present their findings at the Alzheimer’s Association International Conference in London.

Source: WUSTL.

Ideally, a blood-based screening test would identify people who have started down the path toward Alzheimer’s years before they could be diagnosed based on symptoms. NeuroscienceNews.com image is for illustrative purposes only.

Study findings are significant step in predicting disease risk.
Decades before people with Alzheimer’s disease develop memory loss and confusion, their brains become dotted with plaques made of a sticky protein – called amyloid beta – that is thought to contribute to the disease and its progression.

Currently, the only way to detect amyloid beta in the brain is via PET scanning, which is expensive and not widely available, or a spinal tap, which is invasive and requires a specialized medical procedure. But now, a study led by researchers at Washington University School of Medicine in St. Louis suggests that measures of amyloid beta in the blood have the potential to help identify people with altered levels of amyloid in their brains or cerebrospinal fluid.

Ideally, a blood-based screening test would identify people who have started down the path toward Alzheimer’s years before they could be diagnosed based on symptoms.

“Our results demonstrate that this amyloid beta blood test can detect if amyloid has begun accumulating in the brain,” said Randall J. Bateman, MD, the Charles F. and Joanne Knight Distinguished Professor of Neurology and the study’s senior author. “This is exciting because it could be the basis for a rapid and inexpensive blood screening test to identify people at high risk of developing Alzheimer’s disease.”

The findings will be announced July 19 at the Alzheimer’s Association International Conference in London and published online in the journal Alzheimer’s and Dementia.

As the brain engages in daily tasks, it continually produces and clears away amyloid beta. Some is washed into the blood, and some floats in the cerebrospinal fluid, for example. If amyloid starts building up, though, it can collect into plaques that stick to neurons, triggering neurological damage.

A blood test would be cheaper and less invasive than PET scans or spinal taps, but previous studies have found that measures of total levels of amyloid beta in the blood don’t correlate with levels in the brain.

So Bateman and colleagues measured blood levels of three amyloid subtypes – amyloid beta 38, amyloid beta 40 and amyloid beta 42 — using highly precise measurement by mass spectrometry to see if any correlated with levels of amyloid in the brain.

The researchers studied 41 people ages 60 and older. Twenty-three were amyloid-positive, meaning they had signs of cognitive impairment. PET scans or spinal taps in these patients also had detected the presence of amyloid plaques in the brain or amyloid alterations in the cerebrospinal fluid. The researchers also measured amyloid subtypes in 18 people who had no buildup of amyloid in the brain.

To measure amyloid levels, production and clearance over time, the researchers drew 20 blood samples from each person over a 24-hour period. They found that levels of amyloid beta 42 relative to amyloid beta 40 were consistently 10 to 15 percent lower in the people with amyloid plaques.
“Amyloid plaques are composed primarily of amyloid beta 42, so this probably means that it is being deposited in the brain before moving into the bloodstream,” Bateman said.

“The differences are not big, but they are highly consistent,” he explained. “Our method is very sensitive, and particularly when you have many repeated samples as in this study — more than 500 samples overall — we can be highly confident that the difference is real. Even a single sample can distinguish who has amyloid plaques.”

By averaging the ratio of amyloid beta 42 to amyloid beta 40 over each individual’s 20 samples, the researchers could classify people accurately as amyloid-positive or -negative 89 percent of the time. On average, any single time point was also about 86 percent accurate.

Amyloid plaques are one of the two characteristic signs of Alzheimer’s disease; the other sign is the presence of tangles of a brain protein known as tau. David Holtzman, MD, the Andrew B. and Gretchen P. Jones Professor and head of the Department of Neurology at the School of Medicine, is developing a blood-based test for tau that could complement the amyloid test.

“If we had a blood test for tau as well, we could combine them to get an even better idea of who is most at risk of developing Alzheimer’s disease,” Bateman said. “That would be a huge step forward in our ability to predict, and maybe even prevent, Alzheimer’s disease.”
ABOUT THIS NEUROSCIENCE RESEARCH ARTICLE
Funding: This work was supported by the National Institutes of Health (NIH), grant number R01NS065667, and the Alzheimer’s Association Zenith Award Grant, number 3856?80569.
Ovod V, Bollinger JG, Mawuenyega KG, Hicks TJ, Schneider T, Kasten T, Sigurdson W, Sullivan M, Donahue TA, Ramsey K, Paumier K, Holtzman DM, Morris JC, Benzinger TLS, Fagan AM, Patterson BW, and Bateman RJ. Concentrations and Stable Isotope Label Kinetics of Human Plasma Amyloid Beta. Alzheimer’s Association International Conference. Oral presentation. July 19, 2017.
Source: Diane Duke Williams – WUSTL
Image Source: NeuroscienceNews.com image is in the public domain.
Original Research: The study will be presented at Alzheimer’s Association International Conference in London.


http://neurosciencenews.com/alzheimers-blood-test-7128/

Omega-3 Fatty Acids Fight Inflammation via Cannabinoids

NEUROSCIENCE NEWS    JULY 19, 2017

Summary: A new study in PNAS reveals how the body converts omega 3 fatty acids into endocannabinoids, which can have anti-inflammatory effects.

Source: University of Illinois.

Graduate student Josephine Watson, professor Aditi Das, graduate student Megan Corbett, professor Kristopher Kilian and their colleagues discovered an enzymatic pathway that converts omega-3-derived endocannabinoids into more potent anti-inflammatory molecules. Credit: Steph Adams


Chemical compounds called cannabinoids are found in marijuana and also are produced naturally in the body from omega-3 fatty acids. A well-known cannabinoid in marijuana, tetrahydrocannabinol, is responsible for some of its euphoric effects, but it also has anti-inflammatory benefits. A new study in animal tissue reveals the cascade of chemical reactions that convert omega-3 fatty acids into cannabinoids that have anti-inflammatory benefits – but without the psychotropic high.

The findings are published in the Proceedings of the National Academy of Sciences.
Foods such as meat, eggs, fish and nuts contain omega-3 and omega-6 fatty acids, which the body converts into endocannabinoids – cannabinoids that the body produces naturally, said Aditi Das, a University of Illinois professor of comparative biosciences and biochemistry, who led the study. Cannabinoids in marijuana and endocannabinoids produced in the body can support the body’s immune system and therefore are attractive targets for the development of anti-inflammatory therapeutics, she said.

In 1964, the Israeli chemist Raphael Mechoulam was the first to discover and isolate THC from marijuana. To test whether he had found the compound that produces euphoria, he dosed cake slices with 10 milligrams of pure THC and gave them to willing friends at a party. Their reactions, from nonstop laughter, to lethargy, to talkativeness, confirmed that THC was a psychotropic cannabinoid.

Foods such as meat, eggs, fish and nuts contain omega-3 and omega-6 fatty acids, which the body converts into endocannabinoids. NeuroscienceNews.com image is for illustrative purposes only.


It wasn’t until 1992 that researchers discovered endocannabinoids produced naturally in the body. Since then, several other endocannabinoids have been identified, but not all have known functions.
Cannabinoids bind to two types of cannabinoid receptors in the body – one that is found predominantly in the nervous system and one in the immune system, Das said.
“Some cannabinoids, such as THC in marijuana or endocannabinoids can bind to these receptors and elicit anti-inflammatory and anti-pain action,” she said.

“Our team discovered an enzymatic pathway that converts omega-3-derived endocannabinoids into more potent anti-inflammatory molecules that predominantly bind to the receptors found in the immune system,” Das said. “This finding demonstrates how omega-3 fatty acids can produce some of the same medicinal qualities as marijuana, but without a psychotropic effect.”
ABOUT THIS NEUROSCIENCE RESEARCH ARTICLE
The study was an interdisciplinary effort led by recent comparative biosciences alumnus Daniel McDougle and supported by current biochemistry graduate student Josephine Watson. The team included U. of I. animal sciences professor Rodney Johnson; U. of I. bioengineering professor Kristopher Kilian; Michael Holinstat, of the University of Michigan; and Lucas Li, the director of the Metabolomics Center at the Roy J. Carver Biotechnology Center at Illinois.
Das also is an affiliate of the Beckman Institute for Advanced Science and Technology at Illinois.
Funding: The National Institutes of Health and the American Heart Association supported this research.
Source: Aditi Das – University of Illinois
Image Source: NeuroscienceNews.com image is in the public domain.
Original Research: Abstract for “Anti-inflammatory ω-3 endocannabinoid epoxides” by Daniel R. McDougle, Josephine E. Watson, Amr A. Abdeen, Reheman Adili, Megan P. Caputo, John E. Krapf, Rodney W. Johnson, Kristopher A. Kilian, Michael Holinstat, and Aditi Das in PNAS. Published online July 7 2017 doi:10.1073/pnas.1610325114


Abstract

Anti-inflammatory ω-3 endocannabinoid epoxides
Clinical studies suggest that diets rich in ω-3 polyunsaturated fatty acids (PUFAs) provide beneficial anti-inflammatory effects, in part through their conversion to bioactive metabolites.

Here we report on the endogenous production of a previously unknown class of ω-3 PUFA–derived lipid metabolites that originate from the crosstalk between endocannabinoid and cytochrome P450 (CYP) epoxygenase metabolic pathways. The ω-3 endocannabinoid epoxides are derived from docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA) to form epoxyeicosatetraenoic acid-ethanolamide (EEQ-EA) and epoxydocosapentaenoic acid-ethanolamide (EDP-EA), respectively. Both EEQ-EAs and EDP-EAs are endogenously present in rat brain and peripheral organs as determined via targeted lipidomics methods. These metabolites were directly produced by direct epoxygenation of the ω-3 endocannabinoids, docosahexanoyl ethanolamide (DHEA) and eicosapentaenoyl ethanolamide (EPEA) by activated BV-2 microglial cells, and by human CYP2J2. Neuroinflammation studies revealed that the terminal epoxides 17,18-EEQ-EA and 19,20-EDP-EA dose-dependently abated proinflammatory IL-6 cytokines while increasing anti-inflammatory IL-10 cytokines, in part through cannabinoid receptor-2 activation. Furthermore the ω-3 endocannabinoid epoxides 17,18-EEQ-EA and 19,20-EDP-EA exerted antiangiogenic effects in human microvascular endothelial cells (HMVEC) and vasodilatory actions on bovine coronary arteries and reciprocally regulated platelet aggregation in washed human platelets. 

Taken together, the ω-3 endocannabinoid epoxides’ physiological effects are mediated through both endocannabinoid and epoxyeicosanoid signaling pathways. In summary, the ω-3 endocannabinoid epoxides are found at concentrations comparable to those of other endocannabinoids and are expected to play critical roles during inflammation in vivo; thus their identification may aid in the development of therapeutics for neuroinflammatory and cerebrovascular diseases.

“Anti-inflammatory ω-3 endocannabinoid epoxides” by Daniel R. McDougle, Josephine E. Watson, Amr A. Abdeen, Reheman Adili, Megan P. Caputo, John E. Krapf, Rodney W. Johnson, Kristopher A. Kilian, Michael Holinstat, and Aditi Das in PNAS. Published online July 7 2017 doi:10.1073/pnas.1610325114

http://neurosciencenews.com/inflammation-omega-3-cannabinoids-7130/

Several Factors May Predict Cognitive Decline in Parkinson's Disease

July 17, 2017

Up to 80% of patients with Parkinson disease develop cognitive impairment.


Researchers have identified several possible biomarkers of cognitive impairment in patients with Parkinson's disease (PD), according to findings published in PLOS One. These included global atrophy, Alzheimer's pathology, genetic factors, and decreased dopamine in certain areas of the brain.
Up to 80% of patients with PD develop cognitive impairment across multiple cognitive domains. Cognitive decline in PD is most commonly attributed to cortical Lewy body disease, but Alzheimer's disease has been tied to cognitive impairment in PD as well. Further, several risk factors for cognitive decline in PD have been identified, such as age; sex; and subtypes of PD; genetic factors such as apolipoprotein E4, brain-derived neurotrophic factor (BDNF); and diffuse gray matter atrophy.
To better understand biomarkers for early cognitive decline in PD, investigators led by Daniel Weintraub, MD, of the University of Pennsylvania in Philadelphia, analyzed data from the prospective, longitudinal, Parkinson's Progression Markers Initiative (PPMI).
The study included 423 patients with a recent diagnosis of idiopathic PD who were followed for up to 3 years. At the time of enrollment, participants were not treated for PD, did not have a dementia diagnosis, and had decreased dopamine transmission (DaT) on imaging. Potentially predictive biomarkers included structural magnetic resonance imaging (MRI), diffusion tensor imaging, cerebrospinal fluid analysis for amyloid beta, and PD-associated single nucleotide polymorphisms (SNPs).
Cognition was assessed annually with the Montreal Cognitive Assessment (MoCA) test along with tests to assess memory, visuospatial, processing speed, executive function, and working memory domains. A MoCA score <26 was set as the cutoff for cognitive impairment.
Overall, the mean MoCA score decreased by approximately 1 point on average during the 3-year follow-up. This was associated with an increase from 22% to 37% in cognitive impairment and an increase from 1% to 6% in dementia diagnoses.
The biomarkers assessed at baseline did not predict cognitive impairment over time with the exception of participants who demonstrated decreased superior temporal lobe (P =.004) and decreased entorhinal (=.007) thickness on MRI. Likewise, follow-up DaT imaging did not predict cognitive impairment. However, MRI imaging that showed decreased volumes in specific areas of the brain was predictive of a decrease in MoCA scores to less than 26 over time.
After multivariate analysis, biomarkers associated with the prediction of cognitive impairment in patients with PD included dopamine deficiency as evidenced by decreased putamen and caudate DaT; diffuse decrease in cortical volume or thickness in the frontal, temporal, parietal, and occipital lobes on MRI; decreased CSF Aβ 1-42 concerning for Alzheimer's disease pathology; and BDNFval/val and COMT val/val genes.
The study's generalizability was limited by the cohort consisting mostly of white, educated participants and only half or participants having a “research quality MRI scan.”  
“Cognitive decline in early PD is independently predicted by multiple biomarker changes, including nigrostriatal dopamine system deficits, wide-ranging atrophy consistent with cortical neurodegenerative disease, evidence for comorbid AD pathology, and genetic factors,” the investigators concluded.
http://www.neurologyadvisor.com/movement-disorders/identifying-predictors-of-cognitive-decline-in-parkinsons-disease/article/674916/

NICE recommends specialist physio for early-stage Parkinson’s

July 19, 2017

Health professionals should consider referring adults in the early stages of Parkinson’s to physiotherapists for an assessment, education and advice.

NICE recommends the best standard of physiotherapy for Parkinson’s

This is according to an updated guideline from the National Institute for Health and Care Excellence (NICE).
Published on 19 July, the long-awaited document updates a 2006 version and says referrals should be made to physiotherapists with experience in Parkinson’s.
Crucially, physiotherapists should provide information about exercise when offering advice to people in the early stages of the condition, NICE states.
More generally, the guideline recommends that people are offered Parkinson’s disease-specific physiotherapy if they experience balance or motor function problems.
Fiona Lindop, a specialist physiotherapist at Derby Teaching Hospitals NHS Trust, was the only member of the profession on the committee that reviewed the 2006 guidance for more than two years.
Commenting on the update she said: ‘It’s important because if we can assess people early on and identify potential problems, we can improve their quality of life and deal with issues before they become established.’
Research into benefits of physiotherapy
Physiotherapy features in the NICE recommendations for research. It proposes an investigation into whether physiotherapy, started early in the course of Parkinson’s – rather than after the onset of motor symptoms – is beneficial.
NICE says there is no substantial evidence to support the use of physiotherapy at an early stage to stop motor symptoms becoming severe. This is because most trials have involved people who have already developed motor symptoms.
Ms Lindop acknowledged the current lack of evidence, but said it was ‘very exciting’ that NICE had highlighted research into physiotherapy. She added: ‘There are recommendations in the document to help organisations implement the guidance, which is particularly welcome.’
Parkinson’s education
The updated guideline was received positively by Bhanu Ramaswamy, a national project officer for Parkinson’s to ACPIN and Agile, the CSP professional networks for physiotherapists with an interest in neurology and older people, respectively
She welcomed the greater emphasis on the right of individuals affected by Parkinson’s to be involved in discussions and make informed decisions about their care.
Dr Ramaswamy also welcomed the recommendation that physiotherapists should have experience in Parkinson’s, saying this would enable the best standards of physiotherapy intervention to be provided.
‘This ties in with the educational and guideline elements under review through the working groups of the Parkinson’s Excellence Network,’ she said.
http://www.csp.org.uk/news/2017/07/19/nice-recommends-specialist-physio-early-stage-parkinsons

Tuesday, July 18, 2017

Hyposmia: Causes, treatment, and related conditions

Tue 18 July 2017  By Danielle Dresden Reviewed by Stacey R. Sampson, DO 45

Hyposmia is the loss of sense of smell. There are many potential causes for hyposmia, including other health conditions, medication, and head injuries.


Hyposmia is a medical term describing at least a partial loss of the sense of smell. This condition can be both upsetting and dangerous when it occurs.
Estimates suggest that 2 million people or 12 percent of adults in the United States have this syndrome and other disorders that affect their ability to taste and smell.
When people think of the taste or flavor of food, they are considering a combination of sensations, with only some coming from the tongue and taste buds.
he sense of smell contributes greatly to the flavor of foods, as many people will have noticed after a bad cold when food seems to lose its taste. This is why some people with hyposmia think they are suffering from a taste problem when only their sense of smell is affected.

Causes of hyposmia

People can lose some of their ability to smell for several reasons. Possible causes of hyposmia include:
  • allergies
    The loss of sense of smell may be an indication
    of other health conditions, such as Parkinson's 
    disease or type 1 diabetes.
  • head injuries
  • infections, such as the flu
  • small growths in the nose or sinuses, known as polyps
  • deviated nasal septum
Chronic sinus problems, including chronic sinusitis, have also been linked to reductions in the sense of smell.
When the sinuses remain blocked, swollen, and filled with mucus for more than 12 weeks despite treatment, the ongoing inflammation may damage the cells that allow people to smell.
Doctors specializing in conditions affecting the nose maintain that reducing this inflammation can improve the sense of smell.
At least 250 different medications also affect the sense of taste or smell, and some of these drugs can cause hyposmia. They include:
Additional contributors to hyposmia include long-term exposure to certain chemicals, tobacco smoking, or use of recreational drugs, such as cocaine.
Age is another leading factor in a partial loss of the sense of smell. According to the American Academy of Otolaryngology - Head and Neck Surgery, the sense of smell is at its best when people are between 30 and 60 years old. It begins to get weaker after that. Hence, a degree of hyposmia is common in older adults, affecting 39 percent of those over the age of 80.

Related conditions

Hyposmia can also be a sign of other health problems, including:
Most people who have hyposmia will not develop Parkinson's disease. However, the majority of people who have Parkinson's disease, which is a condition of the central nervous system, lose some of their ability to smell.
Due to the link between hyposmia and Parkinson's disease, a test for reduced sense of smell could potentially lead to earlier diagnosis of the disease.
In the case of one of the more common forms of dementia in the U.S, the possibility of using a smell test to screen for early diagnosis is also the subject of ongoing research.
MS is yet another condition that has been associated with hyposmia. A study of people with MS found that 40 percent of its participants had at least a partial loss of their sense of smell. The greater their MS-related disabilities, the more difficulty they had identifying a specific scent.
Multiple studies have found that people with type 1 diabetes can have trouble detecting and distinguishing scents. The more discomfort they had due to diabetic nerve damage, called peripheral neuropathy, the more problems they had with their sense of smell.
Although cancers of the head and neck might not affect the sense of smell directly, irradiation treatment for these conditions can cause some degree of hyposmia.

How might hyposmia progress?

Hyposmia often improves without treatment, particularly if it is caused by seasonal allergies or an infection of the respiratory tract. A person who notices a reduced sense of smell when they have a cold, usually find it returns to normal a few days or weeks after they recover.
When hyposmia is caused by a head injury or a significant inflammatory injury to the cells involved in smell, a complete recovery may not be possible, even with surgery.
However, some medications and retraining of the sense of smell have proven helpful for people with hyposmia.

What is anosmia?

Anosmia is the medical term for complete loss of the sense of smell.
Some people are born with this condition, when it is referred to as congenital. However, it is most frequently caused by head injuries or problems with the nasal passages. These problems can include chronic inflammatory nasal or sinus disease, or a severe viral infection of the upper respiratory tract.
According to the Anosmia Foundation, however, as many as 22 percent of cases of anosmia are idiopathic. This means that no cause can be found for the loss of smelling ability.

When to see a specialist

People have a surprisingly sophisticated sense of smell that can detect from 10,000 to 100 billion different odors. This sensory information plays an important role in supporting a person's quality of life and physical safety.
A medical professional can diagnose hyposmia
by physically examining the nasal passages 
and sinuses.
Enticing aromas encourage people to eat, and nasty smells warn of fire, toxic chemicals or bad food.
Smells also create connections with people and places, say, with the scent of a certain perfume or memories of the seaside or countryside.
When hyposmia limits these abilities, a person must get help immediately to avoid isolation and threats to their physical well-being.
If individuals notice a drop in their ability to smell, they should see a specialist, particularly if the onset of hyposmia is sudden and severe.
The loss of smell can respond well to treatment, especially if it is soon after the problem begins.

Treatment and outlook

Diagnosis and treatment usually begins with a physical examination and check of a person's medical history, especially of upper respiratory problems. A doctor will look at the nasal passages, sinuses, and surrounding structure.
When more detailed images are needed, a nose and throat specialist called an otolaryngologist may conduct a procedure called nasal endoscopy.
In this short procedure, a long thin tube with a camera is inserted into the patient's nose to look at the nasal and sinus cavities.
A doctor will be looking for signs of swelling, bleeding, pus, and possible cancer tumors. Also, they will be on the lookout for other physical blockages that could account for the loss of smell, such as polyps, enlarged nasal structures, or a deviated nasal septum.
If these tests are negative, an MRI scan may be done to look for problems in the areas that detect smells and the brain.
A scratch and sniff test, or tests with "Sniffin' Sticks," helps physicians determine whether someone has anosmia or hyposmia. In cases of hyposmia, these tests will measure the extent of the loss of smell.
On the whole, medication and surgery are used to treat hyposmia. Surgery can be an effective treatment when nasal polyps, a deviated septum, or other problems that can be removed or repaired, are causing the loss of smell.
Medications, such as steroids and antihistamines, may be used to calm the inflammation when allergies or respiratory infections are the cause.
People with hyposmia need to take care to make sure their reduced smelling ability does not cause additional health and safety problems.
It is important to ensure that the loss of smell does not lead to under- or over-eating.
People should make sure that smoke and gas detectors are installed in the household and are well-maintained. To limit the possibility of undetected gas leaks, which are often found by smell initially, people could consider switching from gas to electric appliances.
Using caution when working with potentially toxic household chemicals and keeping a close eye on food expiration dates is also advised.
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