Yes, Wonder Woman really exists and she looks like Jen Parkinson

 On August 15, 2018   By skrischer In Living Well

"Our last name is Parkinson’s, isn’t that why you have it? "      Jen’s 5 year old son

Jennifer Parkinson, yes, that is her real name, is a role model for everyone with Young Onset Parkinson’s Disease (YOPD) and for those of us who are older with PD.  Her story is inspiring,  She is tall, young, beautiful and athletic – Gal Gadot watch out!  And she is the perfect example of how to manage your life while living with Parkinson’s Disease.

We had a chance to meet on Friday morning before the Davis Phinney Foundation‘s Victory Summit in Pasadena, California, where she was scheduled to speak later that day about Women and Parkinson’s Disease.  We initially met almost 3 years ago at a conference sponsored by The Women & PD

Sharon vs Jen

Initiative, which is a program of the Parkinson’s Disease Foundation (now the Parkinson’s Foundation).  Since I was taking boxing classes and Jen teaches boxing, we were asked to give a boxing demo to the other women who attended.  I am the short one in the photo!

On Friday, Jen looked great, no visible tremors or other signs of PD.   Listening to her story, it is hard to believe that this person sitting in front of me went through so much hardship with PD.  Diagnosed 13 years ago at 29, with symptoms that started soon after her son was born, life was not so good.  Jen had a difficult pregnancy, and 6 weeks after her son was born, she noticed a tremor in her right hand.   Even though she was trained as an RN, she never thought that it was PD.  When she went back to work, the shaking made it difficult to work with patients, her writing became illegible, her foot started to shake, making driving difficult, and then her blood pressure started dropping and her heart rate at times went from 30-180.  It was not long before she had to stop working.

“Here’s a prescription, I will see you in 6 months.  Oh, by the way, in 10 years you will be wheelchair bound and unable to take care of yourself or your kids.”

After 2 years of seeing numerous doctors in search of a diagnosis, a visit to an endocrinologist finally put her on the right path.  He sent her to a neurologist that she   worked with at the hospital, who finally diagnosed her with PD.  He put her on Amantadine to see if it would help and said to her:  “Here’s a prescription, I will see you in 6 months.  Oh, by the way, in 10 years you will be wheelchair bound and unable to take care of yourself or your kids.”  Not what she wanted to hear at age 32, with a 2 year old and 5 year old.  He gave her no information, no support groups, nothing about diet or exercise.

She stopped working, went on disability and then got divorced.  She was facing life as a single mother and her symptoms were getting worse, with freezing episodes 2-3 times a day.  She started using a rescue drug that was an injection, but could not administer it to herself since she was home alone.  She often had to wait out the freezing episodes.

That is when she heard about Rock Steady Boxing.  At the time it was only offered in Indiana, so she called a local boxing gym and started training there.  She was training in a regular class with the guys who were getting in the ring.  It was incredibly intense, especially since Jen was the type of person who signed up for the gym but never went until it was time to cancel the membership.  She felt immediate results from the boxing.  She felt good on the days she went to class, and terrible on the other days.

Jen eventually helped set up Rock Steady Boxing with a friend in Costa Mesa, a 2 hour drive from her house.  Soon after, a boxing gym opened up near her.  She went to a class which was taught by her now business partner, Josh.  They eventually opened up a Rock Steady Boxing, and went from 14 to 90 people in a short time.  But they soon realized that they needed more than just boxing classes.  It became clear that support resource for people with Parkinson’s and their families was needed.  And they wanted to open it up to people with other neurologic diseases.  2 years ago, on September 12, 2016, Jen and Josh opened Neuroboxing.  Today they now have 5 locations and also train other trainers to teach neuroboxing.  All of this happened in 2 years.

I asked Jen how she feels.  There are times that are not great, but most of the time she is feeling good.  Her children don’t remember a time that she did not have Parkinson’s.  They remember when she could not get out of bed and when they used to have to help her.  When her son was 5, he once asked if he was going to have Parkinson’s too.  He said:  “our last name is Parkinson’s, isn’t that why you have it?”

When asked if she knew what caused her PD, Jen said that she was in a car accident several months before her symptoms started.  She started having some cognitive issues soon after.  Jen later discovered that 4 other nurses she had worked with at the same facility all have PD.   The nurses are wondering if there was something in the facility that  affected all of them.

Although I had to leave before Jen’s presentation later that afternoon, I hear that she was terrific, inspiring and a true role model.  Our Wonder Woman, Jen Parkinson continues to amaze.

DC Comics Wonder Woman

Thank you to Medtronic, one of the sponsors of the Victory Summit, who arranged for me to meet with Jen at the Summit.  While Jennifer does not have DBS, it has been very beneficial to many other patients with Parkinson’s and Medtronic has a line of DBS systems.

https://twitchywoman.com/2018/08/15/yes-wonder-woman-really-exists-and-she-looks-like-jen-parkinson/

Can Eyes Predict Parkinson’s Disease?

Judy George,08.15.2018

Dopamine loss tied to retinal thinning; may be early disease biomarker

Retinal thinning was linked to dopaminergic neuronal atrophy in a cross-sectional analysis, raising the possibility that it could be a way to detect pathologic changes in early Parkinson's disease (PD) patients, researchers said.

Drug-naïve patients with early Parkinson's showed retinal thinning as measured by optical coherence tomography (OCT) that correlated with both disease severity and nigral dopaminergic degeneration, reported Jee-Young Lee, MD, PhD, of the Seoul National University Boramae Medical Center, and colleagues in Neurology.

"Our study is the first to show a link between the thinning of the retina and a known sign of the progression of the disease -- the loss of brain cells that produce dopamine," Lee said in a statement.

"We also found the thinner the retina, the greater the severity of disease. These discoveries may mean that neurologists may eventually be able to use a simple eye scan to detect Parkinson's disease in its earliest stages, before problems with movement begin."

Retinal pathology has been tied to other neurodegenerative disorders including dementia. In previous studies, retinal nerve fiber layer thickness has been linked to Parkinson's disease, and OCT is a potential PD biomarker.

The search for a definitive Parkinson's biomarker has been extensive and includes clinical (anosmia; REM behavior disorder), genetic (GBA mutation; LRRK2mutation), and biochemical (blood and cerebrospinal fluid) techniques, along with positron emission tomography (PET), magnetic resonance imaging (MRI), and single photon emission computed tomography (SPECT) imaging.

No biomarker has been validated for clinical practice, noted Jamie Adams, MD, of the University of Rochester Medical Center in New York, and Chiara La Morgia, MD, PhD, of the University of Bologna in Italy, in an accompanying editorial: 

"Because of the complexity of the disease, combining biomarkers from different categories is likely the best strategy to accurately predict PD status and progression."

In this analysis, Lee and colleagues studied 49 Parkinson's patients with an average age of 69, along with 54 age-matched controls, including only early-stage, drug-naïve PD patients without ophthalmologic disease.

The researchers used high-resolution OCT to measure retinal nerve fiber layer thickness, microperimetry to measure retinal function, and dopamine transporter analysis to measure N(3-[¹⁸F]fluoropropyl)-2-carbomethoxy-3-(4-iodophenyl) nortropane uptake in the basal ganglia. Retinal layer thickness and volume were measured and compared in PD patients and controls.

Retinal thinning was found in the inferior and temporal perifoveal sectors of the PD patients, particularly the inner plexiform and ganglion cell layers, along with an association between retinal thinning and dopaminergic loss in the left substantia nigra. The team also reported an inverse association between inner retinal thickness in the inferior perifoveal sector and disease severity (Hoehn and Yahr stage), and a positive correlation between macular sensitivity and retinal layer thickness.

"Overall, these data support the presence of an association between retinal thinning and dopaminergic loss in PD," said Adams and La Morgia. "Inner retinal thinning in individuals with PD has been reported in previous studies, but this is the first study that demonstrates a correlation between inner retinal thinning and nigral dopaminergic loss."

"These findings may point to a pathologic connection between the retina and basal ganglia in PD and are in line with previous studies reporting asymmetric retinal nerve fiber layer loss, more evident in the eye contralateral to the most affected body side."

The results need to be interpreted with caution, Lee and co-authors noted. Retina analysis was limited to the macular area in this research. Studies with larger numbers of Parkinson's patients are needed to confirm the findings. And this study was a cross-sectional analysis, so correlations between retinal changes and PD severity need to be established over time.

But if the findings are confirmed, "retina scans may not only allow earlier treatment of Parkinson's disease, but more precise monitoring of treatments that could slow progression of the disease as well," Lee said.

The study was supported by the Seoul Metropolitan Government Seoul National University Boramae Medical Center and the Korean Ministry of Education, Science and Technology.

The researchers reported relationships with Samsung Bioepis and Retimark Inc.

The editorialists reported relationships with VisualDx, Azevan Pharmaceuticals, and Santhera Pharmaceuticals.

https://www.medpagetoday.com/neurology/parkinsonsdisease/74575

FoxFeed Blog: Tests for Parkinson's within Reach

Maggie McGuire Kuhl,      August 15, 2018

Today there are more therapies to slow or stop Parkinson's in human trials than ever before. But those treatments face challenges in proving their effectiveness, and we want to ensure that even more potential therapies enter clinical testing.

Objective, biological markers of Parkinson's disease -- called biomarkers -- would be a game-changer. A perspective published today in the journal Science Translational Medicinelays out the needs and opportunities in Parkinson's biomarker research.

Nearly 40 experts, including Michael J. Fox Foundation (MJFF) CEO Todd Sherer, PhD, and several other senior staff, write that "the creation of tools enabling development of disease-modifying therapies in Parkinson's is a reachable, immediate goal, worthy of research investment." Indeed, MJFF invests significantly in the development of Parkinson's biomarkers, and the ideas in the paper originated from a Biomarkers Discovery Workshop convened by our Foundation in March 2016.

Speeding New Treatments to Patient Hands

The many potential therapies in human testing -- against Parkinson's protein alpha-synuclein, for example, and repurposed from other diseases -- create an urgent need for Parkinson's biomarkers. Most of these trials are following people in the years after diagnosis to see if a drug slows progression of the disease.

The challenge is that people with Parkinson's progress at different rates, so showing a treatment effect is difficult. You may need hundreds of participants observed over multiple years, and a false negative is still possible. If scientists had biomarkers that predicted who would progress faster, they could see an effect sooner and require fewer participants and a shorter study.

The perspective authors point out that the MJFF-led Parkinson's Progression Markers Initiative (PPMI) study shows distinct trajectories of movement symptom decline in early disease, with some progressing much faster than others. Our Foundation is funding PPMI researchers and others to look for biological predictors of those trajectories to help trials choose the fast progressors to test new treatments.

Building on What We Have Now

Some trials are using brain scans of dopamine activity (DAT scans) to help select participants, and last month the European Union's regulatory agency endorsed DAT scan as a tool to enrich Parkinson's trials. However, it's not clear if DAT predicts a person's speed of progression. It shows if someone is experiencing the Parkinson's effect of dopamine loss (as opposed to only exhibiting the clinical symptoms).

It's likely, the perspective authors write, that there will not be one Parkinson's biomarker but a mix of multiple markers that help scientists understand and predict one's experience with disease.

Using Current Resources to Reach Our Goals

Reproducible and accessible biomarkers are possible, the perspective states, because Parkinson's research has built an ecosystem of shared data and biosamples with standardized collection and storage protocols. So scientists have a trove of information to mine and the ability to compare across studies.

Much of this progress happened thanks to PPMI. MJFF launched the study in 2010, and it has since enrolled more than 1,500 people with early-stage Parkinson's, at risk for the disease or without Parkinson's. That set the stage for the Parkinson's Disease Biomarker Program from the National Institute of Neurological Disorders and Stroke (NINDS), part of the National Institutes of Health, and for the Fox Investigation for the New Discovery of Biomarkers (BioFIND), a collaboration between NINDS and MJFF. Other large-scale studies opening access to data and biologics such as fluid and tissue samples have followed.

"Before the advent of these shared biobanks, investigators depended on their own ability to collect hundreds or thousands of samples for testing, preventing potential researchers lacking access to large clinical populations from entering the biomarker discovery arena," said Alice Chen-Plotkin, MD, of the Perelman School of Medicine at the University of Pennsylvania, lead author on the perspective. "However, within the last five years, multiple public-private efforts have laid the groundwork for investigators from both academic and industrial sectors to access well-documented clinical samples. These repositories are all open for collaboration to improve the pipeline to take Parkinson's biomarkers from concept to clinic."

The authors stress the need both for more biomarker discovery efforts and for funding and support of replication and validation studies. Perhaps, they recommend, more clinical trials should release their data. This access would allow scientists to analyze trial results through the lens of emerging biomarkers. 

As the field takes steps toward game-changing Parkinson's biomarkers, "broad collaboration is essential," the authors write. MJFF strives to be a convener in these efforts -- holding workshops to strategize with varied stakeholders, building infrastructure such as PPMI with academic and industry support and funding this important work to ultimately push new treatments to patients sooner.

Read more about the pursuit of Parkinson's biomarkers.

Interested in joining a biomarkers study? Register with Fox Trial Finder to match with clinical studies looking for volunteers like you.

Editor's note: Chen-Plotkin is a member of the MJFF Scientific Advisory Board. Additionally, the ideas in the perspective were further developed in discussions at the NINDS Parkinson's Disease Biomarkers Program annual meeting in August 2016.

https://www.michaeljfox.org/foundation/news-detail.php?tests-for-parkinson-within-reach

First-of-its-kind Parkinson's biomarker guidelines invigorates drive for treatments

15-Aug-2018   University of Pennsylvania School of Medicine

Creating guidelines for discovering Parkinson's biomarkers is key to developing treatments

PHILADELPHIA--Parkinson's disease affects more than 4 million people worldwide, with numbers projected to double in the next few decades. With no known cure, there is a race for treatments to slow or stop the progression of the disease. Key to the research and discovery of treatments for Parkinson's is the identification of biomarkers--a measureable biological indicator, such as proteins found in blood, which can help diagnose disease. 

Today, a slate of guidelines to shape the future of Parkinson's biomarker research have been published in Science Translational Medicine. While previous recommendations have been created to support the research of Parkinson's biomarkers, this is the first developed in collaboration with institutions outside of academic medicine, including The Michael J. Fox Foundation for Parkinson's Research.

Biomarkers can not only help predict, diagnose, or monitor disease, but they can also be used to see how well the body responds to a treatment for a disease or condition. For example, within Alzheimer's disease, measures of the protein beta-amyloid help diagnose the disease, and also serve as a drug target in clinical trials. Similarly, measuring cholesterol levels can help with the diagnosis and treatment of cardiovascular disease. 

Lead author Alice Chen-Plotkin, MD, the Parker Family Associate Professor of Neurology in the Perelman School of Medicine at the University of Pennsylvania, led the project in partnership with experts from 36 organizations, including government groups, academic institutions, and non-profit funding agencies, to foster collaboration and discovery of these critical biomarkers. 

"These players at times have acted in separate worlds, but with a disease affecting so many and lacking in disease-modifying therapies, we're coming together for essential collaboration and innovation," Chen-Plotkin said. "Biomarkers to bolster our efforts to develop new therapies are urgently needed. These guidelines can help make the discovery of biomarkers for Parkinson's a reality."

The guidelines focus on three areas--recommendations for types of biomarkers researchers should identify in order to aid the development of new treatments, resources for collaboration, and research principles to follow.

Previous research efforts have largely focused on biomarkers that distinguish Parkinson's disease from healthy individuals or those with other neurodegenerative diseases such as Alzheimer's disease. However, these guidelines argue for a shift to focus on biomarkers that look within Parkinson's disease itself, as there are many ways the disease manifests in patients. This is an important element for planning clinical trials and developing new treatments. 

Researchers have already built an ecosystem of biobanks at different centers across the world, which hold thousands of biological samples including blood and tissue. These biobanks hold many clues that could help propel the next breakthroughs in the treatment of neurodegenerative diseases, and the guidelines list recommended biobanks as a resource for researcher collaborations. 

"Before the advent of these shared biobanks, investigators depended on their own ability to collect hundreds or thousands of samples for testing, preventing potential researchers lacking access to large clinical populations from entering the biomarker discovery arena," said Chen-Plotkin. "However, within the last five years, multiple public-private efforts have laid the groundwork for investigators from both academic and industrial sectors to access well-documented clinical samples. These repositories are all open for collaboration to improve the pipeline to take Parkinson's biomarkers from concept to clinic."

The guidelines also include recommendations for biomarker research standards, such as larger sample sizes and replication across multiple patient groups. These principles will harmonize findings, streamlining and advancing the biomarker discovery process.

Ideas in the new paper originated from a Biomarkers Discovery Workshop convened by The Michael J. Fox Foundation in New York in March of 2016. They were further developed in discussions at the National Institute of Neurological Disorders and Stroke Parkinson's Disease Biomarkers Program annual meeting in Washington, DC, in August, 2016. 

###

Editor's note: Chen-Plotkin serves on the Executive Scientific Advisory Board for The Michael J. Fox Foundation.

Penn Medicine is one of the world's leading academic medical centers, dedicated to the related missions of medical education, biomedical research, and excellence in patient care. Penn Medicine consists of the Raymond and Ruth Perelman School of Medicine at the University of Pennsylvania (founded in 1765 as the nation's first medical school) and the University of Pennsylvania Health System, which together form a $7.8 billion enterprise.

The Perelman School of Medicine has been ranked among the top medical schools in the United States for more than 20 years, according to U.S. News & World Report's survey of research-oriented medical schools. The School is consistently among the nation's top recipients of funding from the National Institutes of Health, with $405 million awarded in the 2017 fiscal year.

The University of Pennsylvania Health System's patient care facilities include: The Hospital of the University of Pennsylvania and Penn Presbyterian Medical Center -- which are recognized as one of the nation's top "Honor Roll" hospitals by U.S. News & World Report -- Chester County Hospital; Lancaster General Health; Penn Medicine Princeton Health; Penn Wissahickon Hospice; and Pennsylvania Hospital - the nation's first hospital, founded in 1751. Additional affiliated inpatient care facilities and services throughout the Philadelphia region include Good Shepherd Penn Partners, a partnership between Good Shepherd Rehabilitation Network and Penn Medicine, and Princeton House Behavioral Health, a leading provider of highly skilled and compassionate behavioral healthcare.

Penn Medicine is committed to improving lives and health through a variety of community-based programs and activities. In fiscal year 2017, Penn Medicine provided $500 million to benefit our community.

Disclaimer: AAAS and EurekAlert! are not responsible for the accuracy of news releases posted to EurekAlert! by contributing institutions or for the use of any information through the EurekAlert system.

https://www.eurekalert.org/pub_releases/2018-08/uops-fpb081418.php

What long-term cannabis use can do to your brain

Maria Cohut     August 15, 2018

Cannabis use is a topic of fervent debate among researchers. 

As the drug is being legalized in an increasing number of countries, and as its medicinal properties have come into sharp focus, the experts ask to what extent it and its medicinal derivatives are helpful, and to what extent harmful.

A new study warns that long-term cannabis use may harm the brain.

Some use cannabis for recreational purposes, whereas others use cannabis-based drugs or essential oils to relieve chronic pain or treat epilepsy.

Recently, scientists at two academic institutions — Universidade de Lisboa in Portugal and the University of Lancaster in the United Kingdom — have conducted a study into long-term use of cannabis and its potential dangers.

The scientists' findings — published in the Journal of Neurochemistry — indicate that there is one important danger: regular cannabis use could impair a person's memory.

Going forward, as cannabis compounds are increasingly legalized and marketed for therapeutic use, we should consider what the downsides of cannabis use may be and how to address them, says study author Ana Sebastião.

Pitting potential harms against benefits

In the new study, Sebastião and colleagues focused on one cannabinoid-like compound called WIN 55,212-2 and observed its effects on the brain.

The researchers worked with a mouse model and found that, after long-term exposure to this drug, the rodents displayed "significant memory impairments." They were actually unable to distinguish between an object that they should have been familiar with and an object newly introduced to them.

By using brain imaging techniques, the researchers also saw that this drug affects brain regions that are involved in processes of learning, storing, and accessing memories.

Chronic exposure to this substance, explain Sebastião and team, further affects the brain, impairing the "communication" between brain regions that drive learning and memory.

"Importantly," notes Sebastião, "our work clearly shows that prolonged cannabinoid intake, when not used for medical reasons, does have a negative impact in brain function and memory."

"It is important to understand that the same medicine may re-establish an equilibrium under certain diseased conditions, such as in epilepsy or multiple sclerosis, but could cause marked imbalances in healthy individuals."

Ana Sebastião

"As for all medicines, cannabinoid-based therapies have not only beneficial disease-related actions, but also negative side effects," she adds.

A need for preventive strategies

These findings follow from previous research conducted by Sebastião's team, which also found that long-term cannabinoid use affects recognition memory. This is the type of memory that allows us to recall people or things that we have already encountered.

In their other study, the researchers even suggested a way of offsetting this negative outcome: by using a caffeine-related drug.

"These results are very important for the development of pharmacological strategies aiming to decrease cognitive side effects of currently used cannabinoid-based therapies, which proved effective against several nervous system disorders," notes Sebastião.

In the future, the scientists hope that a better understanding of cannabinoid drugs' harmful effects will lead to the development of strategies to counteract them.

"This work offers valuable new insight into the way in which long-term cannabinoid exposure negatively impacts on the brain," says study co-author Neil Dawson.

"Understanding these mechanisms," he adds, "is central to understanding how long-term cannabinoid exposure increases the risk of developing mental health issues and memory problems; only its understanding will allow to mitigate them."

https://www.medicalnewstoday.com/articles/322772.php?utm_source=newsletter&utm_medium=email&utm_country=US&utm_hcp=no&utm_campaign=MNT%20Daily%20Full%20%28non-HCP%20US%29%20-%20OLD%20STYLE%202018-08-15&utm_term=MNT%20Daily%20News%20%28non-HCP%20US%29

What are the symptoms of a UTI in older adults?

Alana Biggers, MD, MPH         14 August 2018

A urinary tract infection (UTI) is a bacterial or fungal infection in part of the urinary system, which includes the kidneys, ureters, bladder, and urethra. UTIs are one of the most common infections in seniors, who can experience more severe symptoms than younger people.

Symptoms of a UTI may include:

• a more urgent need to urinate
• increased urination
• burning, pain, or discomfort when urinating
• feeling pressure in the lower abdomen or pelvis
• cloudy, thick, or odorous urine
• the bladder not feeling empty after urination
• fever
• pain in the lower abdomen, flank, or back
• blood in the urine
• fatigue
• nausea
• vomiting

Older adults are more likely to experience confusion, delirium, or behavior changes in addition to the typical UTI symptoms above.

Symptoms in seniors

Doctors should check for a UTI in any older adults who have a sudden change in behavior or become increasingly confused.

Changes in behavior that may indicate a UTI include:

• restlessness
• hallucination
• social withdrawal
• agitation
• confusion

Why are symptoms different in seniors?

Doctors are not sure why additional symptoms such as confusion or delirium occur in older adults.

One theory is that the blood vessels that supply the brain are weaker and may be more likely to allow the infection to pass to the nervous system.

Causes

Older adults living in long-term care facilities are

 more likely to get UTIs.

Bacteria or fungi that have entered the urinary tract are responsible for causing UTIs.

Many UTIs occur due to E. coli, a type of bacteria that is commonly present in stool and can enter the urinary system through the urethra.

Other organisms that are capable of causing a UTI may be present in older adults who have a catheter or reside in a hospital or care facility.

In fact, UTIs are most common in residents of long-term care facilities such as nursing homes.

What are the risk factors for seniors?

Factors that increase the risk of older adults developing a UTI include:

• changes in the immune system
• exposure to different bacteria in the hospital or care facility
• other health conditions, such as incontinence
• having had a prior UTI
• changes in the way the urinary system works, including prostatic hypertrophy in males
• presence of a urinary catheter, which is a tube that connects the bladder to a bag outside of the body to allow urine to drain

It is important for caregivers to be aware of these risk factors and observe any cognitive changes that could indicate a UTI.

Complications

UTIs are common, but they can potentially lead to severe complications without treatment.

Kidney damage

An untreated UTI can spread to the kidneys and cause kidney damage or disease.

Kidney infections are serious and require intravenous antibiotics and hospitalization.

Sepsis

Another complication of UTIs is sepsis.

Sepsis is a life-threatening condition in which the infection spreads to the bloodstream and then throughout the body. Untreated sepsis can lead to septic shock and eventually death.

Sepsis can cause other complications including organ dysfunction, amputations, and chronic pain disorders. Even if a person has treatment for sepsis, complications may occur.

Treatment

How is it diagnosed?

A doctor may prescribe antibiotics

to treat a UTI.

If doctors suspect that a UTI is present, they will test a urine sample in the office or send it to a laboratory for a urinalysis.

A urine culture can confirm which bacteria are causing the infection. Knowing the specific type of bacteria allows the doctor to determine a suitable treatment plan.

A condition called asymptomatic bacteriuria (ASB) is also common in older adults. ASB occurs when there are bacteria in the urine, but they do not cause any signs or symptoms of infection.

Antipsychotic medications

If a UTI is causing serious delirium or confusion, doctors will use antipsychotic medication until the infection clears. Antipsychotic medicines reduce distress, agitation, and the risk of injury in someone with these types of symptoms.

Intravenous antibiotics

More advanced cases of UTI, such as those that lead to sepsis, septic shock, or kidney infection, may require hospitalization and intravenous antibiotics.

It is common for someone with sepsis or septic shock to have other medical complications that also require medical care.

Can it be prevented?

Taking steps to prevent a UTI is vital for people who have a higher risk of getting one, including older adults.

Methods of preventing a UTI include:

• drinking plenty of fluids
• avoiding caffeine and alcohol
• wiping from front to back after going to the toilet
• promptly changing incontinence pads or underwear when wet

People in a nursing home or long-term care facility often depend on others to take preventive measures against UTIs for them. It is essential that the staff are aware of how to prevent UTIs and understand the signs and symptoms of these infections.

It is important for family members to ensure that older adults have sufficient, appropriate care to meet their needs.

https://www.medicalnewstoday.com/articles/322770.php?utm_source=newsletter&utm_medium=email&utm_country=US&utm_hcp=no&utm_campaign=MNT%20Daily%20Full%20%28non-HCP%20US%29%20-%20OLD%20STYLE%202018-08-15&utm_term=MNT%20Daily%20News%20%28non-HCP%20US%29

LRP10 Gene Variants Implicated in Parkinson Disease, Lewy Body Dementia

Brandon May    August 15, 2018

Investigators found that LRP10 protein localizes to vesicular structures at endosomes, the trans-Golgi network, and plasma membrane of human induced pluripotent stem cell-derived neurons.

Mutations in the LRP10 gene appear to be common in patients with inherited α-synucleinopathies, including Parkinson disease (PD), PD dementia, and dementia with Lewy bodies, according to a study results published in Lancet Neurology. In addition, LRP10 variants correlate with severe Lewy pathology burden in the brain.

A genome-wide linkage analysis of an Italian family (n=10) featuring dominantly inherited PD was performed to identify the PD locus. Investigators also sequenced an international multicenter series comprised of 660 unrelated probands diagnosed with either PD, PD dementia, or dementia with Lewy bodies. Gene sequencing data from patients with abdominal aortic aneurysms were used as controls. In addition, an independent series of individuals with PD and individuals with no signs or familial history of PD or dementia were enrolled and screened for genetic variants.

Significant linkage of PD to chromosome 14 and LRP10 as the disease-causing gene was found in the Italian family. In the unrelated probands, a total of 8 patients carried rare and potentially pathogenic LRP10 variants. In addition, 10 probands with LRP10 variants had a family history of neurodegenerative disease, with LRP10 variants present in 9 of the 10 affected relatives. Definite LRP10 was associated with severe Lewy body pathology in a post-mortem analysis of 3 patients. 

The 3 variants that had a severe impact on LRP10 expression and mRNA stability were 1424+5delG, 1424+5G→A, and Ala212Serfs*17.  In addition, 4 variants affected protein stability, including Tyr307Asn, Gly603Arg, Arg235Cys, and Pro699Ser, whereas Asn517del and Arg533Leu variants affected protein localization. These findings suggested loss of LRP10 function to be a primary driver for pathogenesis.

A limitation of the analysis included the disproportionately greater number of controls enrolled from Taiwan compared with other countries. 

The researchers suggested that future understanding “of the normal function of LRP10 protein and its signaling pathways might offer crucial insights into the molecular mechanisms of inherited, and perhaps sporadic, α-synucleinopathies, pointing to novel biomarkers and therapeutic targets.”

Reference

Quadri M1, Mandemakers W1, Grochowska MM, et al; for the International Parkinsonism Genetics Network. LRP10 genetic variants in familial Parkinson's disease and dementia with Lewy bodies: a genome-wide linkage and sequencing study. Lancet Neurol. 2018;17(7):597-608.

https://www.neurologyadvisor.com/movement-disorders/genetic-variant-implicated-in-parkinson-disease-lewy-body-dementia/article/788284/

What Is It Like to Live with Parkinson’s Disease?

AUGUST 15, 2018  BY "SHERRI WOODBRIDGE"

I read a post recently in a Facebook group for people with Parkinson’s disease. The poster asked fellow group members what their response would be to others when asked what it is like to live with PD. Their answers are incorporated into the column.

Because Parkinson’s is so unpredictable, it is often hard to make definite plans, and you sometimes have to cancel at the last minute. People don’t realize how extreme the pain that comes with this disease can be, and how it can affect your day. You may look good, but you may feel entirely different from the way you look.

Pain has a way of wearing you out and sometimes bringing you down. It can lead to depression, and if you have Parkinson’s disease, you are already more susceptible to depression. It is important to surround yourself with others who are fighting the same fight. Parkinson’s is more than just a movement disorder, and the non-motor symptoms can often be more debilitating than the tremors or dyskinesia.

Stress increases the symptoms of Parkinson’s disease. However, symptoms come and go at varying intensities, so what may be causing you to have a bad day today may disappear tomorrow.

Don’t give up.

At times, not giving up is easier said than done, especially when you feel alone and abandoned. You may feel your friends and family have abandoned you, but it’s often more a case of them not understanding your new journey. It’s probably best to give those people in your life a free forgiveness pass and move on as you make new friends in the PD community who truly understand what living with PD is like.

Parkinson’s disease causes grief, but we can choose to live joyfully and intentionally in spite of what we feel has been taken from us. It is not a death sentence, and we must learn to readjust to our “new” life. And a new life brings new opportunities. As one person said, never lose hope and keep the faith because God is doing miracles every day and you may be the one He is working through to accomplish just that.

***

Note: Parkinson’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. The opinions expressed in this column are not those of Parkinson’s News Today or its parent company, BioNews Services, and are intended to spark discussion about issues pertaining to Parkinson’s disease.

https://parkinsonsnewstoday.com/2018/08/15/parkinsons-disease-patients-share-what-it-is-like-living/