Our Parkinson's Place

WELCOME TO OUR PARKINSON'S PLACE!

I HAVE PARKINSON'S DISEASES AND THOUGHT IT WOULD BE NICE TO HAVE A PLACE WHERE THE CONTENTS OF UPDATED NEWS IS FOUND IN ONE PLACE. THAT IS WHY I BEGAN THIS BLOG.

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 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. IT IS IMPORTANT TO UNDERSTAND I AM A PERSON WITH PARKINSON'S DISEASE. I HAVE NO MEDICAL EDUCATION,

I JUST WANT TO SHARE WITH YOU WHAT I READ ON THE INTERNET. IT IS UP TO YOU TO DECIDE WHETHER TO READ IT AND TALK IT OVER WITH YOUR DOCTOR. I AM JUST THE COPIER OF DOCUMENTS FROM THE COMPUTER. I DO NOT HAVE PROOF OF FACT OR FICTION OF THE ARTICLE. I ALSO TRY TO PLACE A LINK AT THE BOTTOM OF EACH ARTICLE TO SHOW WHERE I RECEIVED THE INFORMATION SO THAT YOU MAY WANT TO VISIT THEIR SITE.

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Sunday, July 24, 2022

Happenings as of July 2022

 July 24, 2022         

My health has been like a roller coaster since December 2020. I have fallen several times. Most of the time I am short of breath. It is hard to exercises on those days. I am officially 73 years old.

I had quite an interested evening a few weeks ago. I was  almost  ready to go to dinner when I began to pick up my foot to put my shoe on, when all of a sudden on the outside near the bottom of my left foot a small vein pop squirting blood everywhere.


We did all of the following:

Elevate your leg above your heart to slow the bleeding. Apply gentle, consistent pressure over the vein. Once bleeding is under control, wrap the vein with a bandage.

We couldn't get the bleeding to stop. My husband called 911. Firemen arrived and it took some time to get the bleeding to stop. They did all of what we did, but wrapped my foot tighter. They instructed me to continue keeping my leg and foot elevated, stating if it begins to bleed again, go to the ER and have them stitch it up. I cancelled the ambulance.

Fortunately it stop bleeding but was quite sore for 3 days. I lost over a cup or more possible close to a pint of blood, my husband said. He cleaned it all up.

The weather here in Southwest Florida has been hot, hot and more hot with the humidity extremely high. This really takes my breath away. So I don't have the energy like I use to. 

I am tired more than normal . I have not been able to exercise like I use to.

I am hoping this weather will improve and I will begin to breath better.

I have not given up.

Monday, February 3, 2020

I want to Inform you of what happened to me.





I went to the hospital by ambulance on December 9th, because I had tremors of my voice box and  the flap suddenly closed. I couldn't breathe and my husband called 911. I went by ambulance and started choking again while being transported to the hospital.



Upon entering the hospital, I stopped breathing again and then went into a seizure like episode. This occurred one more time that evening.

My husband and grandchildren were there. The following day, I had 4 more episodes. My son arrived from Virginia. My husband and daughter called my movement specialist at the University of South Florida, requesting the doctor and giving the neurology department the urgent message. My family called several times, with no response. I slept quite a bit in-between having the episodes. 

My husband stayed 24 hours the entire time not knowing if I was going to live or die. My children also were afraid. Seeing me Choke (not being able to breathe  ) and then having seizure like episodes was quite scary. After that I would fall asleep.

The doctors at the hospital didn't know what to do. The seizure medicine was not working and the problems continued at that time. 



By the third day, I had 3 more episodes, of unable to breathe as well as seizure episodes. My family called my Naples, Florida Neurologist. He immediately spoke to the hospital Neurologist.I was taken off the of the seizure medicine and placed  on a medicine that relaxes the muscles and another drug helping with pain. It worked.  The tremors and choking stopped, and no more seizures.
Thank God.

On the 5th day in the hospital, they released me and placed me in their physical therapy unit. I was there until December 23, 2019.  I did many exercises, including weights, stepping , balance exercises and walking  at a fast pace.  I also completed physical therapy at my home for a month.

I recently had a camera placed down my throat and the tremors are not there since I am taking my PD medicine as well as the new medicine. I do have a bow in my voice box and I am  in the process of checking to find an LSVT Loud in my area. 

I will enroll for that, since the Doctor that performed the test recommended that therapy.  My Naples, Florida Doctor saved me. A Big Thank You goes to Dr. John Campbell   !!!!!!!!

I plan to discontinue this blog, at least for now.


I want to do more things with my family, while I able. There is a part of me, knowing it is hard to say goodbye, so I will say,  "God Bless!"




Monday, December 23, 2019

Where is the news?

December 23, 2019


My first Day in the Hospital !



I AM SENDING MY APOLOGIES TO YOU!

I just returned after 14 days from the hospital, including Therapy.

A nurse will evaluate me tomorrow, Christmas eve, to see what kind of therapy is needed to
get me back to the best I can be.


Dec. 23, 2019


As soon as I can, I  will be back online. Have a very Merry Christmas!

God Bless!

Saturday, December 7, 2019

Understanding What Parkinson’s Progression Means to Each Patient

DECEMBER 6, 2019 BY DR. C




Every day following the ruin of stagnation, it seems that I have progressed from early Parkinson’s to a moderate stage of the disease. But I can’t be sure. Many other factors, including stress, injuries, medication changes, and aging, could be making it look and feel worse. To appease my quandary, I dove into the internet, searching for elucidation about Parkinson’s progression.
We watched as Michael J. Fox and Muhammad Ali were changed by the disease. Granted, their Parkinson’s symptoms were dramatic: Their body movements gradually became less fluid, the tremors more pronounced. Over time, the movement challenges became more noticeable, signifying progression. The Parkinson’s community uses the terms “early,” “middle,” and “late” stage to describe progression. It mostly makes sense and matches what medical providers identify with patients. But it doesn’t help me in my search for well-being possibilities.
Progression for me is more than “early,” “middle,” or “late.” I accept that the disease will cause changes in me and my life. But it would be helpful for my wellness map if some of the pitfalls could be marked, “Danger ahead!” or, “Here’s a list of supplies,” to get me through the hardest parts of my chronic disease journey. Being well-prepared is an essential part of wellness success. The progression of Parkinson’s is not about stages — except in a general way. Rather, it means having some idea about what can be done to slow the progression, or, failing that, how to recognize when progression is happening. Useful information about progression would help guide us through what is sometimes a tortuous journey. It might make the trip easier.
Chatting with the Parkinson’s community reveals the entrenched idea that progression is unique to each person. It would be helpful if our understanding of progression could provide for each patient more details than, “It’s unique to everyone, and you will know when you get there.” So what’s holding up progress toward understanding disease progression?
Medical professionals determine Parkinson’s progression by a system involving a physical exam, patient report, and sometimes a standardized measurement tool or questionnaire. That system fails when all that we are told about progression is, “You’ll know it when you get there.” We need better information from early Parkinson’s stages to understand progression to middle and beyond. Data from the existing collection system is insufficient to give a clear understanding of what progression means to each patient.
I recently read an article in which the authors discuss the merits of the retropulsion test to evaluate postural instability in Parkinson’s. The three methods are: “(1) the pull test as described in the MDS-UPDRS scale; (2) using an unexpected shoulder pull, without prior warning; and (3) the push-and-release test.” Although the test is considered the gold standard, the authors state that “the outcome can vary considerably due to variability in test execution and interpretation.”
The authors state that the test fails to predict future falls, explaining that falling results from the “complex interplay between gait, balance, cognitive decline and environmental factors, and the retropulsion test captures only part of that.”
It is difficult to spot early symptoms during a short office visit once every three to six months. Increasing the speed of care by reducing the duration of clinic appointments has not improved healthcare for this ailing columnist. It hinders the ability of the healthcare practitioner to get to know the patient better and increases the chance of the latter being categorized as “that patient with Parkinson’s.” The provider can’t see all the effects of the chronic disease, even with a longer visit.
We have good and bad days, on and off periods, and life circumstances — all of which make data collection on Parkinson’s progression from a 15-minute office visit problematic. It makes sense that early diagnosis and proper treatment should make a difference in progression. As far as I can tell, no adequate longitudinal studies exist that describe variation in progression as a result of treatment, or lack thereof. This applies even to exercise, my favorite Parkinson’s treatment to slow progression, and the effects of stress as my “most need to avoid” situation to prevent speeding up the progression.
In the next column, I will offer a possible solution to the Parkinson’s progression research problem. 
***
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/2019/12/06/parkinsons-progression-part-1-stages-postural-instability-falls/

Dosing Begins in Phase 2 Trial of CNM-Au8, Potential Therapy for Dopaminergic Neurons

DECEMBER 6, 2019   BY PATRICIA INACIO, PHD




A pilot Phase 2 study evaluating CNM-Au8, an investigational Parkinson’s treatment aiming to protect nerve cells, has started dosing patients, the therapy’s developer, Clene Nanomedicine, announced.
The open-label REPAIR-PD (NCT03815916) clinical trial is enrolling up to 24 people, ages 30 to 80 and diagnosed within the past three years, at its one site at the University of Texas Southwestern Medical Center.
“We are excited to be advancing CNM-Au8 clinically into Parkinson’s patients starting with the REPAIR-PD Phase 2 study” Rob Etherington, president and CEO of Clene, said in a press release.
Parkinson’s disease is characterized by the death of dopaminergic neurons in two brain regions, the striatum and the substantia nigra. These nerve cells rely on large amounts of energy to function, which is provided by mitochondria, the cell’s powerhouses. Failure to provide the energy that cells need contributes to their death.
Oxidative stress, an imbalance between the production of harmful free radicals and the ability of cells to detoxify them, is another hallmark of Parkinson’s disease. These free radicals, or reactive oxygen species, are produced during certain metabolic reactions that involve mitochondria, and can damage cells.
CNM-Au8 is a suspension of nanocrystalline gold designed to increase the production of energy. Specifically, it works by increasing the speed of conversion between two molecules — nicotinamide adenine dinucleotide (NADH) to its oxidized form (NAD+) — resulting in greater production of energy in the form of ATP (adenosine triphosphate, an energy-carrying molecule of cells).
In addition, CNM-Au8 has antioxidant properties that may help to protect cells against oxidative stress.
Preclinical (in the lab) data showed that CNM-Au8 aided the survival of dopaminergic neurons, and helped prevent the loss of mitochondria.
In a rat model of Parkinson’s disease, treatment with CNM-Au8 improved the animal’s motor activity compared to control (untreated) mice. Of note, rats treated with CNM-Au8 in this test showed better results than did rats given carbidopa/levodopa, a standard Parkinson’s therapy.
“Our preclinical data with CNM-Au8 demonstrated improvements in neuronal bioenergetics, which may improve the survival of dopaminergic neurons in patients with PD [Parkinson’s disease], thereby helping slow the progression of this devastating disease,” Etherington said.
A Phase 1 clinical trial involving healthy volunteers (NCT02755870) found CNM-Au8 to be safe.
In the REPAIR-PD study, patients will first undergo a four-week screening period, after which they will drink two ounces of CNM-Au8 daily each morning for 12 weeks. Treatment will be followed by a four-week follow-up period.
The study’s primary outcome is to determine improvements in oxidative stress in the central nervous system (brain and spinal cord), assessed by the ratio of NAD+/NADH measured using magnetic resonance spectroscopy (MRS).
Additional (secondary) measures include assessing the effects of CNM-Au8 on energy production, and nerve cell metabolism.
“The objective of the REPAIR-PD Phase 2 study is to demonstrate improvements in brain bioenergetic metabolism in Parkinson’s disease patients treated with CNM-Au8. Participants will undergo 31phosphorous magnetic resonance spectroscopy (31P-MRS) imaging to show how treatment with CNM-Au8 results in improvements in brain metabolic and membrane biomarkers,” said Robert Glanzman, MD, chief medical officer of Clene.
Results from the REPAIR-PD trial are expected by mid-2020.
https://parkinsonsnewstoday.com/2019/12/06/dosting-starts-phase-2-trial-cnm-au8-potential-dopaminergic-neuron-therapy/

Thursday, December 5, 2019

Exploring the Diversity of Parkinson's Proteins

Dec 05, 2019  Original story from the German Center for Neurodegenerative Diseases





Parkinson’s and multisystem atrophy (MSA) – both of them neurodegenerative diseases – are associated with the accumulation of alpha-synuclein proteins in the brain. Researchers at the German Center for Neurodegenerative Diseases (DZNE) and the Max Planck Institute for Biophysical Chemistry (MPI-BPC) have investigated the molecular makeup of these protein deposits finding structural diversity. Experts from South Korea, Australia, and Argentina were also involved in the study. The results suggest that Parkinson’s might be related to diverse types of protein aggregates.

Alpha-synuclein is a protein that occurs naturally in the body. It is assumed to be involved in signal transmission between neurons. The protein appears both at the cell membrane and solved – floating, so to speak - in the cell’s interior. In addition to these “normal” variants, there are others that manifest in brain diseases. This applies e. g. to Parkinson’s disease and MSA. Both can be associated with various neurological impairments, including movement disorders. In Parkinson’s and MSA alpha-synuclein molecules stick together. As a result, elongated aggregates arise that are deposited inside neurons and other brain cells. “These deposits successively appear in various areas of the brain. They are a disease hallmark,” explains Prof. Markus Zweckstetter, who heads a research group at the DZNE and the MPI-BPC. “There is evidence that these aggregates are harmful to neurons and promote disease progression.”

A matter of folding

These deposits represent a potential starting point for medicines. The idea is that drugs might prevent alpha-synuclein molecules from sticking together or dissolve existing aggregates. To identify potential docking sites for agents, data on the aggregates’ fine structure is required. Thus, the question is: What kind of shape (also known as “folding”) do the molecules adopt within the aggregates? So far, information on this topic had been limited to data from laboratory experiments. “Previous studies investigated the molecular structure of aggregates that were synthesized in a test tube. We asked ourselves how well such artificially produced specimens reflect the patient’s situation. That is why we studied aggregates generated from tissue samples from patients,” said Zweckstetter. “We collaborated closely with international partners on this project. In fact, the tissue samples originated in Australia and the aggregates were synthesized in South Korea. We then did the structural studies in Göttingen.”

Aggregates from brain samples taken from five deceased Parkinson’s patients and five deceased MSA patients were examined. For comparison, the researchers artificially produced different variants of alpha-synuclein aggregates. For this, they used standard procedures. To compare the structure of the different aggregates, they applied nuclear magnetic resonance spectroscopy and other methods.

Structural differences

“We found that aggregated proteins that came from the lab were structurally different to all aggregates generated from patient material,” Dr. Timo Strohäker, first author of the study, commented on the findings. “In addition, proteins of MSA patients differed from those of Parkinson’s patients. If one looks at the data more closely, you notice that the proteins of the MSA patients all had a largely similar shape. The proteins of the patients with Parkinson’s were more heterogeneous. When comparing the proteins of individual Parkinson’s patients, there is a certain structural diversity.”

The alpha-synuclein proteins of all aggregates contain “beta sheets”, which is in line with previous investigations. Accordingly, the molecular backbone is twisted in a way that the proteins are largely two-dimensional. Within the aggregates, the proteins stick together in layers. However, folding does not encompass the whole protein. Each protein also contains areas that are unstructured. Besides, orientation of the beta sheets bears significance. “It is a question of how much of a protein is folded and also how it is folded,” Zweckstetter stated.

Various types of aggregates in Parkinson’s

In the structure of the alpha-synuclein associated with Parkinson’s, there were some significant differences between patients. This might be due to the fact that the course of Parkinson’s can vary quite considerably between individuals. “The variability of Parkinson’s disease could be related to differences in the folding of aggregated alpha-synuclein. This would be in contrast to the ‘one disease-one strain’ hypothesis, that is to say that Parkinson’s disease is associated with one, clearly defined aggregate form. However, in view of our relatively small sample of five patients, this is just a guess,” said Zweckstetter. “Yet, our results certainly prove that studies with tissue samples from patients are necessary to complement lab experiments in a sensible way.”

Reference

Strohäker et al. (2019) Structural heterogeneity of α-synuclein fibrils amplified from patient brain extracts. Nature Communications. DOI: https://doi.org/10.1038/s41467-019-13564-w

https://www.technologynetworks.com/neuroscience/news/exploring-the-diversity-of-parkinsons-proteins-328017

Patent Describes Apple Watch Feature for Improving Treatment of Parkinson's Disease Symptoms

December 5, 2019  by Tim Hardwick (Rumors)

A newly unearthed patent reveals that Apple is exploring how a future Apple Watch could help doctors monitor the symptoms of Parkinson's patients. 


Spotted by AppleInsider, "Passive Tracking of Dyskinesia/Tremor Symptoms" describes the use of special sensors in a proposed ‌Apple Watch‌ medical feature and the reasoning behind it. 
"There are an estimated 600,000 to 1 million cases of Parkinson's Disease in the United States and 60,000 new cases are diagnosed each year," reads the filing, which goes on to describe the symptoms sufferers have to live with. "Symptoms of PD include... tremor and dyskinesia. Dyskinesia is an uncontrollable and involuntary movement that can resemble twitching, fidgeting, swaying or bobbing."
The patent states that dyskinesia and tremors can occur when all of the other features of Parkinson's Disease are being managed through medication. Unfortunately, the dopamine replacement therapy can also cause more pronounced side effects, and doctors have to rely on in-clinic tests and patient reports to regulate their treatment effectively. 
"A patient's quality of life is largely dependent on how precisely clinicians titrate and schedule the patient's medications to minimize the patient's symptoms. This is a challenge for clinicians because each patient has a different combination of symptoms that can change and become more severe over time. Also, in any given day the symptoms may fluctuate based on medications, food intake, sleep, stress, exercise, etc."
The feature uses motion sensors to monitor the wearer's movement and the data gathered is analyzed on the device using the Unified Parkinson's Disease Rating Scale (UPDRS). According to Apple, this allows the data to be collected more reliably and means the sufferer doesn't need to keep close track of their symptoms and can better plan activities around symptom patterns. 

The image above shows a patient wearing an ‌Apple Watch‌, but the patient doesn't specify that the feature would be limited to a wrist-based device, suggesting it could make its way into an iPhone, or perhaps even an electronic finger ring.

https://www.macrumors.com/2019/12/05/patent-apple-watch-improving-parkinsons-symptoms/

Scientists identify chaperones as potential therapies for Parkinson's disease

 December 5, 2019       By Samantha Black, Ph.D.  


University of Basel, Biozentrum

Researchers from the University of Basel have identified the malfunctional relationship and master regulatory mechanisms between chaperone proteins and α-Synuclein occurring in Parkinson's disease. The findings were published in Nature on December 4.
Chaperones are proteins that assist with assembly and disassembly of other macromolecular structures. In humans, chaperones interact with α-Synuclein and the formation of aggregates of intrinsically disordered α-Synuclein, called Lewy bodies, which are strongly associated with Parkinson's disease.
Parkinson's disease is a debilitating neurodegenerative disorder with poorly understood causes. Some are genetic while others are a combination of environmental factors. Regardless of the cause, the disease leads to nerve death within the brain. But with the life expectancy rising around the world, the incidence of Parkinson's disease is projected to increase rapidly in the next years. Therefore, the need for effective therapies is crucial.
Molecular bodyguards interact with α-Synuclein
In the study, the researchers sought to systematically characterize the interaction of molecular chaperones with α-synuclein in vitro as well as in cells at the atomic level. In humans, there are only 30-40 chaperones that could potentially interact with α-Synuclein. They discovered six highly divergent molecular chaperones commonly recognize a canonical motif in α-synuclein and hinder the aggregation of α-synuclein.
"Using state-of-the-art NMR technology, we have discovered a specific pattern that determines the exact interaction site of α-Synuclein with chaperones," explains Sebastian Hiller. "There is not fixed, rigid interaction, but a dynamic and constantly changing encounter."
Impaired chaperone binding causes cell damage
In healthy cells, α-Synuclein is always accompanied by chaperones such that the protein always remains transportable and a pool of functional α-Synuclein proteins is available. Some post-translational modifications of α-Synuclein, such as those observed in Parkinson's disease can interfere with chaperone binding. The researchers found that transient membrane binding triggers a remarkable re-localization of α-synuclein to the mitochondria and concomitant formation of aggregates. Previous research shows that Lewy bodies mainly consist of mitochondrial membrane fragments of α-Synuclein.
New function for chaperones discovered
"With our work, we are questioning the paradigm that the function of chaperones is solely to help proteins to fold into their proper shape," says Hiller. "Chaperones do far more than just assist in protein folding. They control cellular processes by flexibly interacting with a variety of proteins and accompanying them like a shadow." This research helps gain a deeper understanding of the molecular role that chaperones play in cell function and can provide important clues for the development of novel therapies for Parkinson's disease.
https://www.scienceboard.net/index.aspx?sec=ser&sub=def&pag=dis&ItemID=381

Drug helped dementia patients curb their hallucinations and delusions

December 5, 2019

Nuplazid, a drug that treats psychosis in patients with Parkinson’s disease, also curbed hallucinations and delusions in people with dementia, researchers said this week at an Alzheimer’s conference in San Diego.
(Acadia Pharmaceuticals Inc. via Associated Press)


A drug that curbs delusions in Parkinson’s patients did the same for people with Alzheimer’s disease and other forms of dementia in a clinical trial that was stopped early because the benefit seemed clear.
If regulators agree, the drug could become the first offered specifically for treating dementia-related psychosis. It would also be the first new medicine for Alzheimer’s in nearly two decades. 
The daily pill targets some of the most troubling symptoms that patients and caregivers face — hallucinations that often lead to anxiety, aggression, and physical and verbal abuse.
Trial results were disclosed this week at an Alzheimer’s conference in  San Diego.

“This would be a very important advance,” said one independent expert, Dr. Howard Fillit, chief science officer of the Alzheimer’s Drug Discovery Foundation.
Although the field is focused on finding a cure for dementia and preventing future cases, “there is a huge unmet need for better treatment” for those who have it now, said Maria Carrillo, chief science officer for the Alzheimer’s Assn.
The drug, pimavanserin, is sold as Nuplazid by Acadia Pharmaceuticals Inc. It was approved for Parkinson’s-related psychosis in 2016 and is thought to work by blocking a brain chemical that seems to spur delusions.
About 8 million Americans have dementia, and studies suggest that up to 30% of them develop psychosis.
“It’s terrifying,” said Dr. Jeffrey Cummings of the Cleveland Clinic Lou Ruvo Center for Brain Health in Las Vegas. “You believe that people might be trying to hurt you. You believe that people are stealing from you. You believe that your spouse is unfaithful to you. Those are the three most common false beliefs.”
Cummings consults for Acadia and helped lead the study, which included about 400 people with dementia and psychosis. All were given a low dose of the drug for three months, and those who seemed to respond or benefit were then split into two groups. Half continued on the drug and the others were given dummy pills for six months or until they had a relapse or worsening of symptoms. Neither the patients nor their doctors knew who was getting what.
Independent monitors stopped the study when they saw that those on dummy pills were more than twice as likely as those on the drug to relapse or worsen — 28% versus nearly 13%.
There were relatively few serious side effects — 5% in the drug group and 4% in the others. Headaches and urinary tract infections were more common among those on the drug. Two deaths occurred, but study leaders said neither was related to the drug.
Carrillo said the study was small, but the drug’s effect seemed large. It’s unclear whether the federal Food and Drug Administration would want more evidence to approve a new use.
Current anti-psychotic medicines have some major drawbacks and are not approved for dementia patients.
“They’re often used off-label because we have very few other options,” Fillit said.
All carry warnings that they can raise the risk of death in elderly patients, as does Nuplazid.
The drug costs about $3,000 a month, so cost could be an issue. The amount patients pay can vary depending on insurance coverage.
https://www.latimes.com/science/story/2019-12-05/drug-can-curb-dementia-delusions