SENIOR SPOTLIGHT: Memory screenings and 'Cranium Crunches'

 Maureen Wendt Senior Spotlight   January 11, 2019

Maureen Wendt

Most people with dementia remain undiagnosed by their primary care providers, and families often fail to recognize the significance of early cognitive symptoms. Early diagnosis of Alzheimer's disease or other types of dementia is critical. It allows the individual and their family to learn and plan better for the future.

There has been a growing interest in screenings for memory problems. A screening can check a person's memory and other thinking skills. It can indicate whether someone might benefit from a more complete medical visit. Early intervention means better quality of life. A person experiencing changes in memory can improve their ability to manage future affairs by seeking help as soon as possible.

It is important to identify the disease or problem that is causing memory loss. Some memory problems can be readily treated, such as those caused by vitamin deficiencies or thyroid problems. Other memory problems might result from causes that are not currently reversible, such as Alzheimer's disease. In general, the earlier the diagnosis, the easiest it is to treat one of these conditions.

All individuals should be empowered to make informed decisions to better manage their own health, not discouraged from screening based. Memory screenings are a significant first step toward finding out if a person may have a memory problem. Memory problems could be caused by Alzheimer's disease or other medical conditions.

Who should be screened? Memory screenings make sense for anyone concerned about memory loss or experiencing warning signs of dementia; whose family and friends have noticed changes in them; or who believe they are at risk due to a family history of Alzheimer's disease or a related illness.

Questions to ask:

Am I becoming for forgetful?

Do I have trouble concentrating?

Do I have trouble performing familiar tasks?

Do I have trouble recalling words or names in conversation?

Do I sometimes forget where I am or where I am going?

Am I misplacing things more often?

Have family or friends told me that I repeating questions or saying the same thing over and over again?

Have I become lost when walking or driving?

Have my family or friends noticed changes in my mood, behavior, personality or desire to do things?

According to a recent survey by Alzheimer's Foundation of America, 64 percent of individuals who responded to the study thought the behavioral symptoms (such as irritability, anxiety) of the people they were caring for were a normal part of aging prior to their diagnosis of Alzheimer's disease. Sixty-seven percent of these caregivers stated that these thoughts delayed the diagnosis of Alzheimer's disease.

Alzheimer's disease is not a normal part of aging, but age is the greatest risk factor. The number of people with the disease doubles for every five-year age interval beyond 65.

The memory screening test has 80 to 90 percent or higher probability of true or accurate screening results, similar to other established screening tests such as a mammogram and Pap smear.

And, a program for individuals in the early stages of memory impairment is available right here in Niagara County. The dementia-care program emphasizes memory enhancement through cognitive stimulation, education and socialization and is for people in the early stages of memory loss due to Alzheimer's disease, stroke, Mild Cognitive Impairment, Parkinson's disease, or any number of other diseases characterized by memory loss.

Memory Minders, a social program for individuals with mild memory loss, is among The Dale Association's community support services helping to improve the quality of life for adults. For more information about Memory Minders, The Dale Association, or its programs, please contact Angie Blackley at 433-1886, extension 111, or angie.blackley@daleassociation.

Or, if you are looking for a fun way to keep the brain stimulated, maybe "Cranium Crunches" is something for you. Stomach crunches are a basic exercise for abdominal strength. Does that mean that cranium crunches will build strength in your cranium?

You may have heard that the brain is plastic. As you know, the brain is not made of plastic. Neuroplasticity (or brain plasticity) refers to the brain's ability to change throughout life. The human brain has the amazing ability to reorganize itself by forming new connections between brain cells.

For a long time it was believed that as we aged, the connections in the brain became fixed. Research has shown that in fact the brain never stops changing through learning. Plasticity is the capacity of the brain to change with learning. Changes associated with learning occur mostly at the level of the connections between neurons. New connections can form and the internal structure of the existing synapses can change.

Cranium Crunches is one way to use brain plasticity to its capacity, that is, to build your brain. The program uses brain games to stimulate new connections in the brain. It is offered on the third Tuesday of the month from 10 to 11 a.m. at The Dale Association, 33 Ontario St. Please call 433-1886 to reserve your seat for Jan. 15 and you will see that you want to mark your calendar for the third Tuesday of every month.

https://www.lockportjournal.com/news/lifestyles/senior-spotlight-memory-screenings-and-cranium-crunches/article_6972be9c-5c75-5805-9c33-b89139ac67a3.html

10 (Wrong) Things People Somehow Still Believe About Disabled Parking

APRIL 26, 2018

Disability-accessible parking (and the people who use it) is a subject many people feel deserves their attention and judgment. As those who use disabled parking permits know, there are a lot of misconceptions and stereotypes surrounding who “gets” to park in an accessible spot and who must be “faking” their disability in order to park closer to the building.

It’s an issue that never seems to go away. A Twitter user named Daniel Lawson shared a tweet last week claiming, “Disabled parking should only be valid during business hours 9 to 5 Monday to Friday. I cannot see any reason why people with genuine disabilities would be out beyond those times.” While hundreds of people with illnesses and disabilities responded explaining exactly why he was incorrect, it’s still frustrating to hear how misguided people are about accessible parking — and unfortunately, these kinds of attitudes sometimes translate into permit-users being questioned and harassed by people who don’t believe they “really need” their permit.

We wanted to set the record straight on the common misconceptions about accessible parking people still seem to think. Below you’ll find 10 (incorrect) things people somehow still believe about disabled parking — and the truth. With the help of our Mighty community, we break down the frustrating stereotypes and misconceptions, to hopefully help end judgment once and for all.

1. If you’re not using a wheelchair or mobility aid, you don’t need disabled parking.

The truth: Not all disabilities require mobility aids all the time. You can legally get a disabled parking pass even if you don’t use a wheelchair, cane, walker, etc. Some people need passes because they have challenges with breathing or vision, heart disease, fatigue or chronic pain.

“People expect to see some sort of mobility aid, wheelchair, crutches, cane, etc. I’ve been harassed to the point where police have been called because I don’t always use my cane,” said Jessie Lynn Stokes.

“‘You have to be using a wheelchair or cane to use disabled parking.’ On a good day, if I’m not going to be too long, I don’t need my wheelchair but it’s still helpful to be closer to the building,” said Savannah Spigelmyer.

2. Young people who use disabled parking must be faking — only “old people” have disabilities.

The truth: There is no age requirement for getting a disabled parking pass. You can have a chronic illness or disability that would require accommodations at any age.

“Doesn’t happen now I’m in my 60s, but I was stopped by someone when I was young and in my 20s as they assumed that I was faking and didn’t need the wheelchair that I was sitting in!” said Jill Clayton.

“I had a group of elderly women accuse me of using my mother/grandmother’s placard due to my age. I dropped my pants and showed them my surgery scars on my hip and newly replaced knee due to rheumatoid arthritis. I’ve since had two discs replaced in my neck and another knee replacement,” said Amy Kelly.

3. You can park in the crosshatch next to the disabled spot.

The truth: That crosshatch section is not for parking motorcycles, bikes or cars. It ensures people have enough space to get in and out of the car, particularly if they’re using wheelchairs and other mobility aids, or a car with a wheelchair lift. Without the crosshatch, people can become stuck in or out of the car.

“People don’t leave the van accessible spaces open when there are other spaces open and they don’t have a wheelchair van. Also, people will park on the crosshatched area and make it impossible for wheelchair vans to load or unload,” said Caroline Meadowlarke. “I don’t have a wheelchair van, I just try to be respectful for those who do, because their options for parking are even more limited. And that’s what the law is for, disabled parking, anyway.”

4. Disabled parking should only be valid at “certain times.”

The truth: It doesn’t matter what time it is — disabled parking is valid for people who have a disabled parking permit. If someone is “well enough” to go out at midnight, that doesn’t mean they aren’t “really disabled.”

As Twitter user Karrie Higgins wrote in response to Lawson’s tweet above, “We have social lives, jobs, and — wow, this will blow your mind! — we also like to go to arts events, movies, have a drink, eat dinner at restaurants. We are actual PEOPLE! I know that’s MIND BLOWING to you.”

5. You can park in a disabled spot without a pass if you’re “just going to be five minutes.”

The truth: It doesn’t matter how long you’ll be using the spot — if you don’t have a pass, don’t park there. You will be taking a spot from someone who needs it.

As Mighty contributor Paul Eiche, who uses a disabled parking permit for his daughter, wrote, “Disability parking spots, ramps and marked off loading zones are not there for quick stops. They’re not there as reserved areas for everyone’s convenience. They’re there for people who need them. The time may come when you, too, will have need of them, and then you’ll find yourself on the other side.”

6. People who have disabled parking passes are “so lucky.”

The truth: Chronically ill and disabled people don’t use their parking passes “for fun,” they use it because they need it. Telling them they’re “lucky” to have a pass dismisses the challenges they deal with every day.

“[People think] ‘it’s so cool!’ to have a disabled parking permit. No, it’s not. Believe me, I’d much rather not need it. In fact, you can have it if you’ll take this broken body too,” Meadowlarke said.

7. It’s easy to get a disabled parking permit — some people get them even though they’re not “really disabled.”

The truth: In order to qualify for a disabled parking pass, your doctor needs to verify your health condition and that you do have physical limitations that would make a disabled parking permit necessary. There are several steps and paperwork involved with applying for a permit. Of course, fraud does exist, but if a person is using a permit they legally obtained for themselves, then you can rest easy that they do in fact need it.

There are also people who could benefit from a permit, but don’t have one or don’t use their permit even though they need it because they’re afraid of judgment.

“I can’t even get disabled parking when I need it. No doctor will sign off even though I meet the state requirements. Doctors all think I’m ‘too young’ or ‘need to be more mobile.’ It’s the worst being out in the heat for any longer then needed. It’s practically impossible to even get out on a bad day and I hate being an inconvenience to others if I need to be dropped off at the front of places,” said Capri Sprazzle. “I could handle walking from most disabled areas but I’m spent when I end up in the back of the parking lot. It’s really sad that these stereotypes make doctors reluctant to sign the paperwork in the first place.”

8. You’re only allowed to use a disabled placard in one car.

The truth: Disabled license plates cannot be transferred between cars, but disabled placards that hang off the rearview mirror can be used in any car you are currently riding in and will be getting in and out of.

As Lia Seth wrote on HuffPost, “Remember: If you’re ever in the driver’s seat and someone offers you the use of their blue placard, just use it. It’s not illegal or immoral to use it, and your friend has it for a good reason. And if you have one of your own, don’t be afraid to educate your friends about the placard laws, and speak up when you need to use it!”

9. If you can walk at all, you don’t need a disabled permit.

The truth: Many disabled people can walk; however, they may still have pain, fatigue and mobility issues that prevent them from walking the length of a parking lot or from making it back to their car after a long shopping trip. If you see someone walking to or from a car with a disabled placard, that doesn’t mean they are “faking.”

“[People think] if you can walk unassisted you shouldn’t be using it. Usually, I’m OK going into the store, it’s coming back after shopping that makes me so grateful to have my car close,” said Kari Russell.

10. If you are physically able to drive, then you must not be disabled.

The truth: It’s entirely possible to be able to drive but need a disability permit. People who have driver’s licenses and can physically drive a car are not disqualified from receiving a permit. Many people are capable of the physical requirements of driving but have difficulty moving to and from their car. That doesn’t mean they aren’t “really disabled.”

Remember: If you have legally obtained a disabled parking permit, you have every right to use it without shame or judgment. And if you notice someone using a disabled permit, but it doesn’t “look like” they need it, remind yourself that you don’t know their story, and a little understanding and compassion goes a long way.

https://themighty.com/2018/04/disabled-accessible-parking-myths-stereotypes/?utm_source=engagement_bar&fbclid=IwAR1na2lZfjdQYaJVo-oyXvWfHNURkuZowsdXADWEA4HKkr0M6hImGAnLCew

Meditation and Parkinson’s Disease: Looking for Lightness of Being

JANUARY 11, 2019       BY DR. C 

Living with Parkinson’s disease is a struggle against the loss of both motor and cognitive functions. One must invest effort into an action plan that reduces the impact of the disease — a rehab plan. This effort is daily (sometimes hourly) and can be exhausting.

Living with PD is like carrying a large backpack of rocks. It is at times a crushing burden that can overwhelm. Balance needs to be established in my life so that the work I do in fighting the disease does not consume me. I must spend time looking for lightness of being to balance out the heavy PD burden. I do this through a regular practice of meditation.

There are many ways to practice meditation: sitting and listening to calming music, sitting and gazing at a fireplace, practicing tai chi, or exercising with rhythmic breathing. These practices seek to help one enter the quiet mind. It is within the quiet mind that one experiences lightness of being. Meditation helps relieve stress and focus attention — both of which are of benefit to those with PD. There are books providing instructions on how to do this, but none deal directly with PD.

Practicing meditation with PD presents some unique challenges. The meditation practice starts with calming the body, and this is the first obstacle PD complicates. Repetitive motor activities like cycling, tai chi, or gardening are helpful when combined with focused breathwork.

Focused breathwork is diaphragm breathing in which you focus your full attention on the breath. Guided meditation, either from a teacher, in person, or from a recording, can help with this process of shifting attention. This shifting of attention is the second obstacle PD complicates.

Once past the first two obstacles, you should feel a little more relaxed. This relaxed state is the path leading to the door into the quiet mind, but I am prevented from going down that path by a third obstacle.

This third obstacle is heightened emotions and difficulty in regulating them. I have written about how PD heightens the impulse signals to the brain. During the meditation process, the signal-to-noise ratio changes, meaning that as one practices quieting the mind, the noise goes down and the signals connected to emotion appear louder.

The quiet mind is a mental state that silences the noise of the world, the body, and the self while at the same time maintaining a sense of peace and safety. It is something I practiced for decades and then lost touch with over the last seven years while battling PD. As my life has become stable, I am now returning to the practice and finding it much more difficult. I feel like a novice struggling with all the obstacles I used to walk around with ease. This third obstacle does impede my looking for lightness of being.

As I have helped patients to find a place of peace and safety, together we would often experience loud emotions. These are emotions connected to things we feel (consciously or subconsciously) that need attention. They are like boulders in the path, looking like obstacles blocking the way forward to the quiet mind. But one can learn to walk around them.

Most of the folks I worked with would have several boulders to walk around and needed multiple sessions to learn how to walk around them. As I write this, I remember the tender patience I should offer to myself.

Once past the boulders of emotion, you then arrive at the doorstep of the quiet mind. PD has made looking for lightness of being much more difficult for me, but not impossible. I have memories, and recently have felt glimpses of peace and deep calmness.

Seeking lightness of being ties into my New Year’s resolution. For me to quiet down the old tapes (emotional boulders in the path), I need to have a new mental state to go to. I can’t just remove the tapes and leave a void, because that void will be quickly filled back in with the old mental habits. Looking for lightness of being will be a lifetime adventure.

What ways do you practice meditation, and how have you found it to be helpful?

***

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/2019/01/11/meditation-parkinsons-disease-looking-lightness-of-being/

Abnormal Brain Cell Type Leads to Parkinson’s-Related Neurodegeneration, Study Contends

JANUARY 11, 2019      BY CATARINA SILVA IN NEWS.

Scientists have found that an abnormal version of brain cells called astrocytes contribute to the accumulation of alpha-synuclein protein, the main component of Parkinson’s disease hallmark Lewy bodies.

Their study, “Patient-specific iPSC-derived astrocytes contribute to non-cell autonomous neurodegeneration in Parkinson’s disease,” was published in Stem Cell Reports.

Parkinson’s disease is linked to degeneration of the ventral midbrain (relating to the inferior part of the brain), a region that houses dopamine-releasing neurons.

Post-mortem analysis of Parkinson’s disease brain tissue has revealed astrocytes accumulate toxic amounts of alpha-synuclein during the disease process. Research also suggests that this toxic protein can be taken up and spread from astrocytes to neurons, causing neuronal death.

Astrocytes are star-shaped cells that outnumber neurons by fivefold. Found in the central nervous system, astrocytes are known as housekeeping cells because they care for neurons, nurture them and “clean up” after them.

Investigators set up to further investigate a role for Parkinson’s disease-related astrocyte dysfunction in midbrain nerve cell death.

They generated astrocytes and ventral midbrain dopaminergic neurons from induced pluripotent stem cells (iPSCs) of healthy individuals and of patients with the LRRK2G2019S mutation, the most commonly found mutation in Parkinson’s disease.

iPSCs are derived from either skin or blood cells that have been reprogrammed back into a stem cell-like state, which allows for the development of an unlimited source of almost any type of human cell needed.

Although LRRK2’s main function is not known, it seems to play a key role in mitochondria — cells’ powerhouses — namely in autophagy, a process that allows cells to break down and rebuild their damaged components.

Healthy neurons and Parkinson’s astrocytes were together in the same lab dish to study their cellular interactions. Results revealed a significant decrease in the number of healthy ventral midbrain dopaminergic neurons when cultured together with Parkinson’s disease astrocytes, which was associated with astrocyte-derived alpha-synuclein aggregation.

Healthy neuronal death was caused by the shortening and disintegration of the cells’ projecting branches, known as axons and dendrites.

When healthy astrocytes were cultured with Parkinson’s neurons, the housekeeping cells partially prevented the appearance of disease-related cellular changes and alpha-synuclein buildup in the diseased neurons.

“We found Parkinson’s disease astrocytes to have fragmented mitochondria, as well as several disrupted cellular degradation pathways, leading to the accumulation of alpha-synuclein,” the study’s co-first author Angelique di Domenico, PhD, said in a press release.

Because Parkinson’s astrocytes had high levels of alpha-synuclein in them, researchers hypothesized that the toxic protein could be transferred to healthy dopamine-producing neurons and cause the damage they had previously observed.

Using the CRISPR-Cas9 gene editing tool, the team generated two new astrocyte lines (representing one Parkinson’s patient and one healthy control). This allowed them to “tag” alpha-synuclein within living cells and track the protein as it was generated by astrocytes and transferred to dopamine-producing neurons.

As expected, alpha-synuclein in Parkinson’s astrocytes accumulated at abnormally high levels and, upon culture with healthy dopamine-producing neurons, a direct transfer of astrocytic alpha-synuclein to neurons was observed.

Researchers then used this gene-editing technology to generate Parkinson’s astrocytes that lacked the LRRK2 G2019S mutation. Abnormal alpha-synuclein accumulation did not occur in gene-corrected astrocytes and upon culture with healthy neurons, there was no accumulation of alpha-synuclein or decrease in neuron survival.

Researchers then treated Parkinson’s astrocytes with a chemical designed to correct the cells’ disrupted clean-up system.

“We were elated to see after treatment that the cellular degradation processes were restored and alpha-synuclein was completely cleared from the Parkinson’s disease astrocytes,” di Domenico said. “These results pave the way to new therapeutic strategies that block pathogenic interactions between neurons and glial cells.”

https://parkinsonsnewstoday.com/2019/01/11/defective-glial-cells-push-neurons-toward-parkinsons-desease/

Genetic Variant Predetermines Risk of Cognitive Decline in Parkinson’s, Research Suggests

 JANUARY 11, 2019 BY CATARINA SILVA 

Researchers have found that Parkinson’s patients whose cognitive ability is intact, but who have a specific genetic variant, have significantly less gray matter in the regions of their brain that are related to dementia.

The study with that finding, “Reduced gray matter volume in cognitively preserved COMT 158Val/Val Parkinson’s disease patients and its association with cognitive decline,” was published in Brain Imaging and Behavior.

Several mutations in the COMT gene have been associated with the risk of developing Parkinson’s disease. This gene provides instructions for making catechol-O-methyltransferase (COMT), an enzyme that helps break down certain chemical messengers like dopamine.

The most common alteration in the DNA sequence that makes up the COMT gene is the Val158Met mutation in which a valine (Val) is replaced by a methionine (Met) at position 158. Val and Met are both amino acids, also known as the protein’s building blocks.

Every individual has two copies of each gene, one inherited from each parent. Therefore, a person can have two Val’s in the same position at both COMT gene copies (also known as the Val/Val genotype), a Val in one gene and a Met in the other (Val/Met genotype), or two Met’s (Met/Met genotype). Scientists use the word “genotype” to describe a person’s genetic constitution.

Changes in COMT’s molecular structure, lead to high (Val/Val), intermediate (Val/Met) and low (Met/Met) enzymatic activity.

The Val158Met mutation in the COMT gene has been associated with an increased risk of cognitive decline in Parkinson’s disease, particularly in people with greater COMT activity. When this happens, there is too much neurotransmitter degradation, thus leading to reduced levels of dopamine and affecting basic brain functions such as motor coordination and memory.

Evidence suggests a correlation between cognitive impairment, one of Parkinson’s non-motor features, and reduced gray matter volume.

The brain is composed of gray and white matter. The first consists of cell bodies — the control center of neurons — while the latter is made up of nerve cell projections, known as axons or fibers, connecting distinct parts of gray matter.

A Spanish team of researchers used magnetic resonance imaging (MRI), a non-invasive imaging technology, to investigate a possible structural brain compromise in Parkinson’s patients with highly active COMT activity that could explain their increased risk for subsequent cognitive impairment.

The study included 120 newly diagnosed Parkinson’s patients with normal cognition (who were not previously treated for the disease) and 48 healthy controls from the Parkinson’s Progression Markers Initiative database.

Results showed that there was a widespread, significant reduction in cerebral gray matter volume in patients with the Val/Val genotype. They observed alterations in the fronto-subcortical and posterior-cortical brain regions, where motor and cognitive functions originate.

Gray matter volume at some of the identified regions was associated with cognitive decline in a four-year follow-up period, suggesting that gray matter volume reduction during the early stages of disease predisposes Val/Val patients to cognitive impairment.

Nonetheless, gray matter volume analysis at one-year follow-up was not increased in Val/Val subjects, in comparison to Val/Met and Met/Met participants, indicating a somewhat stable atrophy in the Val/Val subset and that those brain changes might already be present prior to diagnosis.

The team believes their research “sparks the need to further characterize the association between a modified COMT enzymatic effect and a structural brain compromise in the early stages of [Parkinson’s disease].”

https://parkinsonsnewstoday.com/2019/01/11/genetic-variant-predetermine-cognitive-decline-parkinsons/

Changes in Gait, Cognition May Be Early Signs of Idiopathic Parkinson’s, Research Suggests

JANUARY 10, 2019 BY CATARINA SILVA 

Changes in gait and cognition precede a diagnosis of idiopathic (without known cause) Parkinson’s disease, and may occur earlier than typical non-motor symptoms, a study has found.

The study, “Prediagnostic markers of idiopathic Parkinson’s disease: Gait, visuospatial ability and executive function,” was published in Gait & Posture.

Motor symptoms in idiopathic Parkinson’s disease (IPD) are identified relatively late in the disease course, reducing the odds of neuroprotective benefit from available treatment options. Identifying individuals during the prodromal (early) period that precedes motor symptoms could be of great use for clinical studies seeking new therapies to prevent or delay disease progression.

A team of French researchers sought to determine the existence of any subtle gait disorders or other signs that precede the diagnosis of IPD, based on data from a long-standing study of human aging across the adult lifespan: the Baltimore Longitudinal Study of Aging (BLSA).

Conducted by the National Institute on Aging (NIA) Intramural Research Program, the BLSA continuously enrolls healthy volunteers age 20 and older who are followed throughout their life independently of the development of age-related diseases.

Ten pre-diagnosed IPD patients (eight men and two women) and 30 healthy control subjects were chosen for this study.

Subjects were assessed for the disease approximately 2.6 years before diagnosis. Clinical examination included gait speed, spatio-temporal gait parameters, balance, upper-limb motor skills, neuropsychological profile, and non-motor symptoms.

In comparison to the control group, IPD patients had shorter step length and reduced gait speed in a usual gait speed testing condition. Despite also having shorter step length when testing maximum gait speed, no differences between the IPD and control samples were found in walking speed.

Moreover, patients had worse mental rotation ability (the ability to rotate mental representations of two-dimensional and three-dimensional objects, which is related to the brain’s capacity for visual representation), and impaired ability to name different examples that could be inserted into a category (for instance, naming all types of flowers one can think of in one minute).

Compared to control subjects, IPD patients had no changes in upper-limb motor function, no depression, no sleep disturbances, no urinary symptoms, and no orthostatic hypotension (when blood pressure suddenly drops when standing up quickly).

Researchers concluded that the observed “changes might serve as markers to improve the early detection of IPD patients, who could then benefit from pharmacological neuroprotection trials and/or prevention trials of lifestyle-related interventions in order to delay, or even prevent, clinical manifestations.”

https://parkinsonsnewstoday.com/2019/01/10/change-gait-early-sign-idiopathic-parkinsons-disease-study/

Inbrija Approved in US to Treat Off Periods in Parkinson’s Patients on Carbidopa/Levodopa

 JANUARY 10, 2019 BY JOSE MARQUES LOPES, PHD IN NEWS.

The U.S. Food and Drug Administration has approved Inbrija (levodopa inhalation powder)‎ for the treatment of Parkinson’s off periods in patients on a carbidopa/levodopa regimen.

Acorda Therapeutics’ therapy is expected to be available by prescription in the first quarter of 2019. It will be distributed through a network of specialty pharmacies in the U.S.

“Today’s approval of INBRIJA marks a major milestone for both Acorda and the Parkinson’s community, for whom we are gratified to have developed this much needed therapy,” Ron Cohen, MD, Acorda’s president and CEO, said in a press release. Cohen noted the more than “two decades of research and development” needed for this approval, as well as the “enormous perseverance and ingenuity” by Acorda’s team.

Inbrija is a self-administered, orally inhaled levodopa treatment for off periods, which are characterized by the re-emergence of Parkinson’s motor symptoms due to low levels of dopamine between doses of standard treatment. These off episodes are typically more common as the disease progresses.

The Michael J. Fox Foundation helped to fund the early development of Acorda’s medication, a decision based on the impact off periods have on patients’ lives, according to Todd Sherer, PhD, the foundation’s CEO.

“We knew we had to help address this unmet need, and this approval is a significant step forward for the community as it provides a new option to manage these gaps in symptom control,” he said.

Inbrija uses Acorda’s ARCUS technology, a system designed to deliver medication to the lungs through inhalation. ARCUS transforms molecules into a light, porous, dry powder, enabling the delivery of much higher doses of medication.

The FDA’s decision was based on a clinical program that included approximately 900 Parkinson’s patients. The pivotal Phase 3 SPAN-PD trial (NCT02240030) evaluated the efficacy and safety of 84 mg and 60 mg of Inbrija in 351 participants with mild to moderate Parkinson’s who were experiencing off periods.

Results of the double-blind study showed a statistically significant improvement in motor function at the final 12-week visit, seen by a reduction in the Unified Parkinson’s Disease Rating Scale Part III (UPDRS-III) score with Inbrija’s higher dose, compared with placebo, at 30 minutes post-dose. Inbrija’s effects were seen as early as 10 minutes after treatment.

The most common adverse reactions with Inbrija were cough, upper respiratory tract infection, nausea, and discolored sputum, which may indicate a bacterial infection.

Treatment with Inbrija was also analyzed in a one-year, randomized, open-label Phase 3 trial with 398 participants (NCT02352363). Results showed a similar average reduction in forced expiratory volume in one second — a measure of pulmonary function — in the Inbrija (84 mg) and observational groups.

Inbrija also eased Parkinson’s symptoms at all time points, as measured with the UPDRS-III scale, enabled symptom control within 60 minutes of the dose and reduction of total daily off times, and led to improved Patient Global Impression of Change scores in 75% of patients, which reflects the patients’ assessment of treatment effectiveness.

“In the clinical study program, Inbrija established its safety profile and demonstrated clinically meaningful improvements in motor function,” said Robert A. Hauser, MD, a professor of neurology and director of the Parkinson’s Disease and Movement Disorders Center at the University of South Florida. “Inbrija helps address a significant unmet need for people with Parkinson’s, and we look forward to adding this new treatment option to our armamentarium.”

Inbrija is not to be used by patients currently on or treated with a nonselective monoamine oxidase inhibitor, such as the antidepressants and anxiolytics phenelzine or tranylcypromine, within the last two weeks.

The company is currently seeking EU approval for Inbrija.

Burkhard Blank, MD, Acorda’s chief medical officer, said he was “delighted” with Inbrija’s approval and its upcoming availability for on-demand use, based on each patient’s needs.

“We thank the FDA for a constructive dialogue throughout the development program and their partnership during the review cycle. We especially thank all those who volunteered for the Inbrija clinical trials, without whose commitment new medications could not be developed,” he said.

He further noted the important role played by “people living with Parkinson’s, their care partners, researchers, clinicians and advocacy groups,” to achieve FDA approval.

A webcast of a recent conference call hosted by Acorda is available here:

http://ir.acorda.com/investors/investor-events/event-details/2018/Acorda-Therapeutics-Conference-Call-dec-2018/default.aspx

https://parkinsonsnewstoday.com/2019/01/10/fda-approves-inbrija-treatment-off-periods/