Aspen Neuroscience Receives $6.5M to Advance New Patient-specific Cell Therapy for Parkinson’s

Aspen Neuroscience

Aspen Neuroscience, a new biotech company, has raised $6.5 million to develop cell therapies for Parkinson’s disease using patients’ own cells.

The company was co-founded by renowned stem cell scientists Jeanne F. Loring, PhD, and Andres Bratt-Leal, PhD, and initially supported by Summit for Stem Cell, a non-profit organization that provides a variety of services for Parkinson’s patients.

Parkinson’s hallmark motor symptoms include tremor, slowness of movement (bradykinesia), stiffness (rigidity), uncontrollable movements (dyskinesia), and poor balance.

As the disease progresses, patients typically need to gradually increase their dopaminergic therapeutic dose for maximum benefit. Even after that they might sometimes experience reappearance or worsening of symptoms due to diminishing effects of dopaminergic therapy, known was “off” periods.

Importantly, dopaminergic therapy is delivered to areas of the brain other than the striatum, a key motor control region severely affected in Parkinson’s disease. Because of the therapy’s off-target behavior, patients also may experience side effects such as hallucinations or cognitive impairment.

Aspen wants to combine its expertise in stem cell biology, genomics and neurology and develop the first autologous (self) stem cell-based therapy for Parkinson’s disease.

In this type of cell therapy, a patient’s own cells (usually skin cells) are reprogrammed back into a stem cell-like state, which allows the development of an unlimited source of almost any type of human cell needed, including dopamine-producing neurons, which are those mainly affected by this disorder.

Because these cells are derived from patients, they do not carry the risk of being rejected once re-implanted, eliminating the need for immunosuppressive complementary therapies, which carry serious side effects such as infections and possibly limiting therapeutic potential.

In theory, replacing lost dopaminergic neurons with new stem cell-derived dopamine-producing ones could potentially ease or reverse motor symptoms associated with the disease.

Aspen is developing a restorative, disease modifying autologous neuron therapy for people suffering from Parkinson’s disease,” Howard J. Federoff, MD, PhD, Aspen’s CEO, said in a press release.

“We are fortunate to have such a high-caliber scientific and medical leadership team to make our treatments a reality. Our cell replacement therapy, which originated in the laboratory of Dr. Jeanne Loring and was later supported by Summit for Stem Cell and its President, Ms. Jenifer Raub, has the potential to release dopamine and reconstruct neural networks where no disease-modifying therapies exist,” Federoff said.

The company’s lead product (ANPD001) is undergoing investigational new drug (IND)-enabling studies for the treatment of sporadic Parkinson’s disease. Aspen experts also are developing a gene-editing treatment (ANPD002) for familial forms of Parkinson’s, starting with the most common genetic variant in the GBA gene, which provides instructions to make the enzyme beta-glucocerebrosidase.

The new seed funding round was led by Domain Associates and Axon Ventures, with additional participation from Alexandria Venture Investments, Arch Venture Partners, OrbiMed and Section 32, according to the press release.

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Could It Be the Pseudobulbar Affect or Am I Just Happy?

pseudobulbar affect

I was playing a nice, calm game of Hearts with my kids and grandkids when I started laughing. Again. My outburst was not out of the ordinary, unless somewhat irrepressible mirth counts as abnormal.

I’ve experienced several bouts of uncontrollable laughter in the last few months. I have noticed that it happens during my exercise class, when I’m with family, and at other times. People usually think that I am up to something. But I am not, I just can’t help smiling.

The pseudo … what?

The pseudobulbar affect (PBA) is a condition sometimes seen in people with Parkinson’s disease. It is distinguished by a loss of control when it comes to laughing or crying. One moment the person with PBA is sitting with you, having a normal conversation, and the next, they are laughing or crying uncontrollably. At least that’s how I would imagine it would play out. Their outbursts don’t correspond to the emotions they are displaying; for example, laughing when they’re grieving, or crying when they’re telling a joke.   

So, does smiling count when it comes to the pseudobulbar affect? I don’t usually indulge in self-diagnosis, and I’m not looking to entertain another disorder. However, I find this condition to be fascinating. 

With Parkinson’s disease, we are often battling a “stone face” and trying to find our lost smiles. I have experienced both ends of the smile spectrum. I have had people admonish me, telling me to smile, when I am having a perfectly super day, but my smile — or lack thereof — seems to suggest otherwise. Equally, I have received several compliments from people saying that I have a beautiful smile. 

What to do?

I have learned while attending physical therapy to do everything BIG and intentionally — as I wrote in my column, “I’ve Made BIG Improvements with Parkinson’s Therapy Program.” I believe that smiling is just as important as good balance. Your smile is often your calling card in life.

I don’t believe that I have PBA — but who knows? Perhaps it is the beginning of this strange condition, but I don’t think so. I smile because I am happy and filled with unspeakable joy. And I don’t intend to wipe that feeling off my face anytime soon.


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.

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Report Highlights Potential Benefits of Drinking Coffee in Neurodegenerative Diseases, Including Parkinson’s


Drinking coffee regularly may help reduce the risk of neurodegenerative diseases — including Parkinson’s disease — particularly in men, according to a new report from the Institute for Scientific Information on Coffee (ISIC).

With the substantial improvements in medical care, health, and quality of life over the past decades, global life expectancy has risen to 72 years (latest data, 2016), according to the World Health Organization.

Nevertheless, longer life expectancies come with increased risk of disease and disabilities. It is estimated that up to 10 million people worldwide are living with Parkinson’s disease, the second most common age-related neurodegenerative disease after Alzheimer’s.

Increasing evidence suggests that lifestyles — such as diet, caffeine/coffee consumption, and smoking — may contribute to people’s risk of developing Parkinson’s and other neurodegenerative conditions.

In particular, previous preclinical studies have shown that some coffee components (caffeine combined with EHT, and phenylindane) can prevent the formation of the toxic protein aggregates associated with Parkinson’s development.

The ISIC’s new report discusses the association between dietary components, particularly coffee and its components, and a reduced risk of neurodegenerative disorders, including Parkinson’s and Alzheimer’s.

The report was written by Elisabet Rothenberg, PhD, a dietitian and an associate professor at the Food and Meal Science department of Kristianstad University, Sweden.

While the link between diet and Parkinson’s disease is still largely ambiguous, likely due to underlying genetic and gender-specific factors, increasing evidence suggests that diet and dietary compounds may influence the risk of developing the disease.

A recent review study highlighted the potential protective effect of a Mediterranean diet, uric acid, good polyunsaturated fats, coffee, caffeinated tea, as well as beer in Parkinson’s development, particularly in men. Uric acid is an antioxidant molecule formed with the break-down of purines, which are compounds found in several foods, including liver, shellfish, sardines, and alcohol.

Meanwhile, other data suggest that consumption of dairy products and saturated fats may increase Parkinson’s risk.

The first reports about coffee consumption and the lower risk of Parkinson’s were published in the 1970s. Since then, several studies have analyzed its potential protective properties.

Available data suggest that drinking coffee reduces the risk of developing Parkinson’s disease by up to 30%, in a dose-dependent manner, with most studies indicating three cups of coffee as the beneficial dose. However, the best dose of coffee and caffeine consumption is still unclear.

Besides its potential effect on the risk of Parkinson’s disease, coffee consumption also has been suggested to help ease Parkinson’s symptoms both in animal models and in patients.

Several studies also have highlighted that men may benefit more than women from being coffee drinkers, with some studies showing an up to 60% reduced risk of Parkinson’s disease among male coffee drinkers.

This potential gender-specific benefit may be explained by underlying hormonal and genetic factors and/or the lower frequency of Parkinson’s disease among women. Preclinical studies in mouse models of the disease suggest that a competition between estrogen and caffeine may be behind this gender difference.

Notably, while some studies have found an association between the non-use of postmenopausal hormones and coffee drinking in the reduction of Parkinson’s risk in women, more recent studies have shown the opposite trend.

Overall, additional studies are required to better understand these potential associations and their underlying mechanisms, as well as to clarify gender differences and interactions between hormones and coffee compounds.

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Things Lost and Things Gained

Have you ever heard someone say that having Parkinson’s can be blamed for much and many a thing? I have. And why not blame our woes on this disease? It’s taken much and many a thing from us. Things we, at one time in our lives, had full control over. Things about which we had some say. 

Parkinson’s disease (and other various diseases some people don’t know ‘what to do with’) can be blamed for from the loss of things physical, to the loss of things emotional. For troubles encountered in the financial realm, to the loss of things we must struggle with in the mental. It can be responsible for the loss of relationships, to the loss of joy and happiness we once cherished and held dear.

Things lost.

Broken marriages.


Pain and fears without names.

Can this disease also be blamed for the loneliness you feel, standing deep within a crowd? Are we able to blame tears we cannot control or screaming we cannot contain on something we cannot see – this thing we call a ‘disease’? I say – yes.

In its clutches we can feel as if we are being tossed about within and then turned from the  inside to out.

It often seems as if all we do is done the wrong way. The masked look on our face is constantly being misunderstood. There are things we can’t say and there are things we cannot do. We would if we could but no more are they ours to accomplish on our own. 

Our legs won’t get us where we want or need to go – fast or safe enough. Our fingers will not move our pen across pages we yearn to fill.

Can we really blame Parkinson’s for all that garbage and pain? I’d like to believe that’s a choice we do have, to blame it all on a disease that steals and destroys, leaving us powerless and literally, without much of a voice of our own.

I don’t know why a select group – a band of brave warriors and/or a flock of faithful friends – have been chosen to ‘endure for a cure’. I do know that it is only by sticking together that we will make it through.

In the gamut of things gained, we step back and wonder, what is it that we have reaped through pain and suffering, if anything?

Things gained

‘Pay it forward’ was a common phrase a while back, the idea being if someone did something kind for you, you would hopefully pay the kindness forward to someone else. Think about that in the realm of Parkinson’s disease and things gained. 

In no way do I mean pay pain and suffering toward someone else! Instead, pay forward what we have learned from this disease. The encouragement, the wisdom, and the knowledge that we can offer to others. Those who are not as far along as we.

It is a kindness we all can share and share in, in spite of what we have lost. 

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Devices to Record the Progression of PD


The progression of Parkinson’s disease (PD) is unique to every person, with different early, middle, and late-stage symptoms. However, this view of PD progression may be an artifact of limited data rather than an accurate description. We need new ways of measuring PD symptoms as they change over time. We have the technology to create new devices that people can use over an extended period, across multiple settings and severity of “off periods.”

I see progression as a change in the intensity and duration of “bad” days and off periods. Many longitudinal studies investigate the progression of PD (for example, the rate of progression in exercise), but it is hard to find studies that measure changes in response to treatment. Devices discussed in this column might change that.

Better measurement of PD progression begins with a few assumptions. First, subtle, early motor symptoms will appear before more obvious symptoms, such as tremors or bradykinesia. Second, early motor symptoms will be inconsistent and episodic. Third, we have the technology to build mobile monitoring devices.

I recently read that a patient being evaluated for “internal tremors” showed no signs of tremor during a physical examination of his bare feet. However, once he put his socks and boots on, an astute clinician observed the left bootlace swinging in such a way that, when measured, fit the PD pattern of a tremor. In other words, while the patient didn’t exhibit tremor during a visual examination of his bare feet, his shoelace reflected an underlying tremor!

A shoelace is not going to be a reliable measuring device, but it proves that slight motor changes that are difficult to detect do exist. I’ve designed two possible motor symptom detection devices: a mobile swing monitor (MSM) and a fine motor skills test (FST). Both devices would record and monitor movement fluctuation over time and across settings in daily life over 10 or so days. Both devices use sensors to track and record movement through three dimensions.

The MSM uses five “movement in 3D space” sensors — one on each wrist, one on each ankle, and one on the belt — with recording hardware for all five. Worn for several days, like a Holter monitor, the MSM would map the sway of the arms, legs, and body over time and across settings. The MSM is very similar in appearance to wearable training weights, which can measure the slightest variations in body movement. Wearable training weights are used by Olympic and World Cup judges to evaluate Shaun White’s amazing snowboard flips and twists.

The FST, illustrated in the graphic below, has a 3D monitor in the “soda can” receptor where the block is inserted. Similar to the game “Operation,” the patient must remove objects from openings in the receptor without setting off the buzzer. The warning light goes off when the sensor plate is touched.

The FST will measure how the person adjusts position and control while using fine motor skills. The FST uses a 3D monitor and four independent, pressure-sensitive plates that record when the patient fails to insert the block and when the block is aligned. The plates can be positioned at different widths using an adjustable difficulty setting, making it harder to insert the block without touching the plates.

Fine skills motor test, designed by Dr. C. (Photo by Dr. C)

Data gathered by these two devices may provide patients and medical professionals with more accurate clinical data about motion, tremors, and fine motor skills over a greater period. They could demonstrate the progression of intensity and duration of bad days and off periods and serve as the beginning of a database on PD progression.

Many people are excited about using technology to provide outcome measures. As we know, technology is not being utilized in offices with patients to help understand the progression of PD. But hopefully, that will change.

If these devices are already being tested in the home of PD patients, sign me up!


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.

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Personalized Brain Maps May Help Improve Deep Brain Stimulation for Parkinson’s, Other Conditions

deep brain stimulation

Not everyone’s brain connections map at exactly the same location, which may explain why deep brain stimulation (DBS) therapy, used for severe cases of Parkinson’s and other neurological conditions, works for some patients and not for others, a study has found.

The findings,”Integrative and Network-Specific Connectivity of the Basal Ganglia and Thalamus Defined in Individuals,” could improve DBS treatment for Parkinson’s patients, by helping doctors choose where in the brain to implant electrodes based on each patient’s own brain maps. The research was published in the journal Neuron.

DBS — a surgical procedure in which electric stimulators are placed at target regions inside the brain — may be used to relieve motor symptoms in some people with Parkinson’s, who have had the disease for at least four years and whose motor symptoms cannot be fully controlled by medication.

It usually works best to ease stiffness, slowness, and tremor, and not as well for imbalance, sudden inability to move when walking, or non-motor symptoms.

For other neurological conditions, DBS can be used to ease cognitive symptoms such as obsessive thoughts and compulsive behaviors.

However, this method is not effective for all patients. In the case of Parkinson’s, it can be transformative for some, but for others, it causes side effects that outweigh the benefits, including worsened thinking or memory problems.

“Deep-brain stimulation is a very invasive treatment that is only done for difficult, severe cases,” one of the study’s leaders, Deanna Greene, PhD, a professor at Washington University School of Medicine in St. Louis, Illinois, (WUSTL) said in a press release.

“So it is difficult to grapple with the fact that such an invasive treatment may only help half the people half the time,” Green said.

She and her colleagues mapped specific circuits in the brain using magnetic resonance imaging (MRI) and found that each person’s brain networks position a bit differently. This may help explain why the effects of DBS vary so much from person to person and point to a potential way of improving the treatment.

It all started when a group of scientists from Washington University scanned themselves at night as part of the so-called Midnight Scan Club.

From the brain scans of 10 healthy individuals, researchers created three-dimensional maps of the functional networks running through structures located deep inside the brain, which usually are targeted by DBS and known as the thalamus and the basal ganglia.

Both these regions have been linked to neurological and psychiatric conditions, but so far the precise mapping of its activity has been  challenging technically.

Researchers discovered that the distinct networks that control vision, movement, attention, goal-directed behaviors, or the brain’s default state at rest, mingle and share information at nine hubs inside the basal ganglia and thalamus.

Importantly, they saw that each person’s functional networks can be positioned a bit differently, so when DBS electrodes are placed in the same anatomical spot they may influence different functions in different people.

Some networks and their connecting spots — such as the motor integration zone, where the control of movement and goal-directed behavior share paths — maintained pretty much the same location in all people. Of note, these regions corresponded to “consistently successful sites of deep brain stimulation,” the researchers wrote.

“I showed a neurosurgeon where we’d found the motor integration zone, and he said, ‘Oh, that’s where we put the electrodes for essential tremor, and it always works,’” said the study’s senior author, Nico Dosenbach, MD, PhD, and a professor at WUSTL.

Conversely, other networks and intersection points — some targeted to treat Parkinson’s disease — varied significantly more from person to person.

“We saw that there was a great deal of variation across people in terms of what functional networks are represented there, and deep-brain stimulation is only about 40% to 50% successful there,” Dosenbach said.

The team is now exploring ways of using each person’s brain map to personalize the best regions to target to provide relief while avoiding side effects. They also want to look for other brain spots that might provide even better results.

“What this study suggests is that a particular patient may do better if the wire is placed in relation to their personal functional brain map rather than in context of the population average. A personalized functional map — as opposed to an anatomical map, which is what we use today — could help us place a wire in the exact place that would provide the patient with the most benefit,” said study co-author Scott Norris, MD, professor at WUSTL.

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Parkinson’s Foundation Adds 5 Sites to Its Free Genetic Testing and Counseling Effort

free genetic testing program

The Parkinson’s Foundation announced that it has added five sites to its national initiative that provides complimentary genetic testing and counseling to people with Parkinson’s disease (PD).

In addition to helping patients better understand their disease, the program aims to improve Parkinson’s therapies — and enable personalized treatments — by advancing research into its genetic origins and differences.

The new PD GENEration: Mapping the Future of Parkinson’s Disease sites are Massachusetts General Hospital, Northwestern Medicine in Chicago, Struthers Parkinson’s Center at Park Nicollet in Minnesota, the University of California San Diego, and the Perelman School of Medicine at the University of Pennsylvania.

They join Columbia University Irving Medical Center in New York, initiative’s first site.

All are part of the Parkinson’s Foundation Centers of Excellence network, made up of 48 leading medical centers worldwide, including 34 in the U.S. that treat more than 185,500 PD patients.

This pilot study’s goal is to enroll 600 people. Longer term goals are to establish 50 Centers of Excellence and Parkinson Study Group sites in the U.S. that can provide testing and counseling to some 15,000 Parkinson’s patients.

“Through the PD GENEration program, we can continue to improve Parkinson’s care by accelerating and supporting research,” said John L. Lehr, president and chief executive officer of the Parkinson’s Foundation, in a press release. “We are thrilled to expand this unique initiative that offers the Parkinson’s community the opportunity to learn more about their diagnosis while helping scientists advance the understanding of the disease.”

Investigators will use test results in work to develop better PD therapies and personalized medicine. Understanding genetic differences across those with Parkinson’s can help reveal necessary clues about how and why each patient’s disease experience differs.

Another study goal is to encourage patients to take part in clinical trials based on their test results. Genetic tests for Parkinson’s are now either unavailable or unaffordable, and largely not covered by private health insurance. In many cases, genetic counseling is not included.

“This program will help us better understand how people with Parkinson’s experience symptoms and respond to treatments related to this disease so that scientists can start building the foundation for precision medicine in PD,” said James Beck, PhD, the foundation’s chief scientific officer. “Now, even more people with PD will have better access to their genetic data through their clinicians.”

Enrollment sites and contact information for the PD GENEration program can be found here. The main criteria for participation is a confirmed PD diagnosis. All data shared with the research community will be kept confidential, the foundation states.

“This is an exciting time for patients and clinician scientists as the genetic advances in Parkinson’s disease are allowing us to develop targeted therapies,” said Anne-Marie Wills, MD, an assistant professor of neurology at Massachusetts General Hospital.

“This large-scale genetic screening initiative will enable patients and their providers to identify genetic mutations which can lead to personalized treatments for people with Parkinson’s disease. We applaud the Parkinson’s Foundation in their efforts to move the field forward,” Wills added.

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3D Structure of Brain Alpha-Synuclein More Heterogeneous Than Previously Thought, New Study Reports

Alpha-synuclein aggregates

Clumps, or aggregates of alpha-synuclein protein in the brain, a hallmark of Parkinon’s disease, are more heterogeneous than previously thought, according to a new study. Moreover, the protein’s 3D-structure is different in Parkinson’s patients as compared with lab-made versions.

These findings may hold implications for the development of treatments targeting alpha-synuclein, as new therapies need to take into account what kind of shape the protein adopts within nerve cell aggregates.

The study, “Structural heterogeneity of α-synuclein fibrils amplified from patient brain extracts,” was published in the journal Nature Communications.

Parkinson’s disease and multisystem atrophy (MSA) belong to a class of neurodegenerative disorders called synucleinopathies that are characterized by the accumulation of misfolded alpha-synuclein proteins.

These abnormal protein aggregates are toxic, and mainly accumulate in Parkinson’s disease in dopamine-producing nerve cells — those responsible for releasing the neurotransmitter dopamine. Dopamine is a chemical messenger that allows nerve cells to communicate and, among other functions, helps regulate movement.

“These deposits successively appear in various areas of the brain. They are a disease hallmark,” Markus Zweckstetter, a professor and research leader at the German Center for Neurodegenerative Diseases (DZNE) and the Max Planck Institute for Biophysical Chemistry (MPI-BPC), said in a press release.

“There is evidence that these aggregates are harmful to neurons and promote disease progression,” he added.

Given the key role of alpha-synuclein aggregates in the development and progression of Parkinson’s disease and other neurodegenerative disorders, these protein clumps represent potential therapeutic targets. Treatments could either prevent the aggregates from forming or eventually clear them from within the brain.

To identify which specific sites on alpha-synuclein can be targeted by potential therapies, researchers need to have an understanding of the complex structure these proteins acquire once they form aggregates. However, current knowledge is limited to aggregates that are established in the lab, in a test tube, which may be different from what actually happens in patient’s brains.

“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,” Zweckstetter said.

Zweckstetter and his team collaborated with researchers in Australia and South Korea to analyze the structure of alpha-synuclein aggregates derived from brain samples of individuals with Parkinson’s disease (five patients) and MSA (five patients). They then compared them to those artificially produced in the lab.

The brain samples were taken from a region of the brain called the amygdala, which plays a key role in regulating emotions and memory, and is known to be affected in Parkinson’s.

The brain-derived alpha-synuclein aggregates were structurally different to those generated in the lab, the researchers found.

Alpha-synuclein proteins found within aggregates contained a structure known as “beta sheets”— whose orientation was of relevance — and their molecular backbone was twisted in a way that the protein was mainly two-dimensional. That is in contrast with a three-dimensional structure.

Within aggregates, alpha-synuclein proteins stick together in layers. However, this folding was not seen across the whole protein, with certain areas remaining unstructured.

The scientists also found that alpha-synuclein aggregates from Parkinson’s patients showed more diverse structures than those from people with MSA. That may reflect “the greater variability of disease phenotypes [manifestations] evident in PD [Parkinson’s disease]”, the researchers said.

“Proteins of MSA [multisystem atrophy] 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,” said Timo Strohäker, first author of the study.

The researchers noted that “although larger patient numbers are required to link [alpha-synuclein] aggregate structure with symptomatic heterogeneity of the disease, our data point to the possibility that [alpha-synuclein] aggregate structure could be specific for individual patients or certain subtypes of [Parkinson’s disease].”

The findings of differently structured alpha-synuclein proteins among different Parkinson’s patients contrasts with current hypotheses theorizing that each neurodegenerative disease is associated with a single, defined structure of alpha-synuclein protein.

“The variability of Parkinson’s disease could be related to differences in the folding of aggregated alpha-synuclein,” Zweckstetter said. “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,” he added. “Yet, our results certainly prove that studies with tissue samples from patients are necessary to complement lab experiments in a sensible way.”

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Defects in Molecular Chaperones May Help Drive Lewy Body Formation in Parkinson’s, Study Finds

Lewy bodies, Parkinson's

Defects in chaperone proteins that interact with alpha-synuclein and work as a type of “molecular bodyguard” may help drive the formation of Lewy bodies, which are a hallmark of Parkinson’s disease.

The findings were published in the journal Nature, in a study titled “Regulation of α-synuclein by chaperones in mammalian cells.”

Lewy bodies are protein aggregates — basically clumps of improperly folded protein — that are often found in the brains of people with Parkinson’s disease. The main protein that forms Lewy bodies is alpha-synuclein. However, what drives alpha-synuclein to form Lewy bodies is an area of ongoing investigation, which may open avenues for the development of treatments.

In this new study, researchers investigated not alpha-synuclein itself but its so-called chaperones. Traditionally, “chaperone” proteins are thought of as proteins that temporarily bind to other proteins to help them fold properly.

The researchers screened dozens of known chaperones in detail to see whether they could interact with alpha-synuclein.

“[W]e have discovered a specific pattern that determines the exact interaction site of [alpha]-synuclein with chaperones,” study co-author Sebastian Hiller, a professor at the University of Basel, said in a press release.

Hiller and colleagues identified six that can interact with alpha-synuclein. Many of these were heat shock proteins, a well-established family of chaperones.

The researchers then set about inhibiting the interaction between alpha-synuclein and its chaperones. They found that, upon blocking this interaction, chaperones could no longer act as “molecular bodyguards” and protect alpha-synuclein, which tended to accumulate in the mitochondria — cells’ powerhouses — where it aggregated, forming clumps of protein that bear a striking resemblance to Lewy bodies.

“Our results establish a master regulatory mechanism of [alpha]-synuclein function and aggregation in mammalian cells,” the researchers said.

While this study doesn’t definitively prove that abnormally functioning chaperones are responsible for Parkinson’s, it suggests that the chaperone system plays a role in the progression of the disease — and, as such, it could be a target for future therapies.

These findings also have implications for the broader biological understanding of what chaperone proteins do.

“With our work, we are questioning the paradigm that the function of chaperones is solely to help proteins to fold into their proper shape,” Hiller said. “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.”

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My Favorite Holiday Gift Ideas for Your Loved Ones with Parkinson’s

Christmas gift ideas

Every year, I compile a list of holiday gift ideas for people with Parkinson’s disease. This year, I’ve taken my favorites from previous lists and added some new ideas. I’m offering them here for those who need assistance with finding the right gift for their loved one.

A few of my favorites

Two of my all-time favorites are a terry cloth bathrobe and an electric toothbrush. The robe can be worn after showering when we don’t have the strength to dry ourselves or struggle with balance. A task like brushing our teeth doesn’t have to be so difficult when we have a quality battery-powered toothbrush.

Years ago, I bought a herbal neck wrap. I heat it in the microwave and use it to relieve stiffness in my neck. I also lay it across my feet to warm them up. These wraps are super easy to make: Use corn or rice and mix in aromatic herbs such as lavender.

For the love of books

If your loved one enjoys reading, a Kindle or another e-reader could be the answer to your gift-giving question. Fine motor skills — such as turning pages — can be challenging for some people with Parkinson’s. And a touch screen could be the solution. You could add a gift certificate to cover their first book purchase.

Personal care tasks, such as taking care of nails, become more difficult as the disease progresses. Your loved one might be delighted with a voucher for a professional manicure. A basic treatment is not overly pricey and often includes a hand massage. You could splurge and add a pedicure to make them feel truly pampered.

An alternative to a professional manicure is a do-it-yourself nail painting that an older grandchild could give to a grandparent. People with Parkinson’s might be grateful for an electric manicure set if they can still take care of their nails.

Let’s admit it: Some tasks would be easier with help, but you’d like to maintain your modesty a little longer. Have you considered a bidet toilet attachment? I discovered this device a few months ago and thought, “Why not?”

Following are more gift ideas that may inspire you this holiday season:

  • Slipper socks with nonslip soles to prevent falls;
  • Gift certificates for dance, voice, or other Parkinson’s-specific classes;
  • A Rock Steady Boxing membership;
  • Weighted eating utensils;
  • Book of puzzles or brain teasers;
  • Colored pencils and adult coloring books.

Whatever you decide to give your person with Parkinson’s, if the gift is chosen with love, they will appreciate it.


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.

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