Genervon Presents Future Goals for Investigational GM6 Therapy in Parkinson’s, Other Diseases

genervon

Genervon Biopharmaceuticals announced its future goals for investigational therapy GM6 in a recent presentation on its multi-target drug development strategy to tackle neurodegenerative diseases, including Parkinson’s disease.

Genervon presented its hypothesis that a multi-target drug approach is the key to curing complex neurological disorders at the 2018 BIO CEO & Investor Conference on Feb. 12, 2018, at the New York Marriott Marquis.

Following this strategy, researchers at Genervon previously discovered what they believe is the regulator of the development of the human nervous system, called the motoneuronotrophic factor (MNTF).

The company then developed GM6, a synthetic equivalent of MNTF, and launched a comprehensive clinical program to test GM6 as a potential treatment for Parkinson’s disease and other central nervous system (CNS) diseases.

Phase 2 trials are now being planned to test GM6 in Alzheimer’s disease, Parkinson’s disease, Huntington’s disease, and multiple sclerosis.

MNTF is an endogenous neurotrophin — a growth factor that induces the survival, development, and function of neurons — highly specific of the central nervous system and expressed rapidly during the first three months of human embryonic development of the complete nervous system, peaking at week nine and remaining detectable in adult tissue.

Previous studies showed that MNTF regulates embryonic stem cell differentiation into motor neurons and helps maintain these nerve cells. Additionally, MNTF helps motor axon regeneration and restoration of nerve function in target muscles and organs.

GM6 controls the development, monitoring, and correction of the human nervous system. It can traverse the blood-brain barrier — a highly selective membrane that helps shield the brain and central nervous system from blood circulation — and activate an embryonic program to help detect and repair damages to the central nervous system, including those triggered in Parkinson’s and other neurodegenerative diseases.

Genervon’s pre-clinical studies identified six potential mechanisms of action of GM6 in Parkinson’s disease, including the down-regulation or up-regulation of six genes involved in signalling, growth factor generation, or oxidative stress defense.

In 2013, Genervon launched a Phase 2a clinical trial (NCT01850381) to assess GM6’s safety and tolerability in Parkinson’s disease patients.

The pilot study enrolled six patients, who were randomized to receive either intravenous GM6 and a placebo. They received six doses of GM6 or placebo over two weeks. Researchers measured the levels of brain-derived neurotrophic factor (BDNF), a blood marker for Parkinson’s disease, at the start (visit one), after four doses (visit four), after six doses (visit six) and 10 weeks post-treatment (visit eight).

Changes in BDNF blood levels for each patient relative to baseline were analyzed at visits four, six, and eight. The results showed that GM6 was well-tolerated and linked to favorable changes in BDNF.

GM6 has also been granted orphan drug status and a fast-track designation by the U.S. Food and Drug Administration to treat amyotrophic lateral sclerosis (ALS), and a Phase 3 trial is being planned to test GM6 in ALS.

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Depression in Parkinson’s Is Not Something to Clown Around About

depression

Sherri Journeying Through

You’ve just returned home from school. A conference. A training course. And now, what is one of the first questions you might be asked?

Did you learn anything?” or “What did you learn?”

I remember coming home from elementary school and being asked by my uncle, “Did you learn anything?” No. No, I didn’t. That was my usual response because day after day that’s how it felt. But day after day, eventually you realize you are learning. Something.

I was asked that question regarding a seminar I attended a while ago.

Did you learn anything?” Yes. Yes, I did.

Anna Sanger Reed, one of the staff members at the Parkinson’s Resources of Oregon, came from Portland to Southern Oregon to teach a “Parkinson’s Disease 101” event. She gave an overview of Parkinson’s disease (PD), which included general information regarding what PD is and who may be a likely candidate. She went over the symptoms of PD, treatments, and therapies available to patients and other resources that are currently available.

Anna mentioned a study on depression in Parkinson’s patients and the results showed the disease progressing faster when depression is involved. (Sorry, I didn’t get the name of it, but this 2009 study shares similar info, and this site has great info on the effects of depression on PD.) It makes you want to become a clown or buy one and have them around. Maybe not. Many people are scared out of their wits by clowns. I guess they can be intimidating with that big hair, those big lips, the big shoes, and always hiding behind a painted face.

So, I guess that would be the “anything” I learned, which when I think about it, was a good thing to learn. Because so many people can battle depression in Parkinson’s disease, it’s important to know if you’re one of those people. Do you feel down or blue much of the time for no apparent reason? Do you feel lifeless or tired, like you’re dragging? Do you have a lack of energy and just want to crawl back into bed (if you even got out of bed) and go back to sleep with the pillow over your head? Are your thoughts focused on defeat instead of hope?

Because depression, in a sense, can be life-threatening, it’s important to be aware of any signs that are obvious (and not so obvious) that show you may be struggling in this darkness and seek help from your doctor right away. It would most likely be a better option than buying a clown because sometimes clowns can be very, very scary. Yes. Yes, indeed.

***

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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8 Common Treatments for Parkinson’s Disease

Parkinson’s disease is a long-term degenerative disease that affects the central nervous system. To date, there is no cure for the condition, but there are medications and therapies available to address some of the symptoms and improve quality of life for patients.

Here are eight of the main drugs and therapies used in the treatment of Parkinson’s disease, according to the Mayo Clinic:

MORE: Discover 10 early signs of Parkinson’s disease

1. Carbidopa-levodopa: Levodopa is a naturally occurring chemical which can enter the brain and be converted to dopamine when combined with carbidopa. The carbidopa also prevents the levodopa from converting into dopamine before it enters the brain.

The is one of the most effective treatments for Parkinson’s although after long-term use, the effects start to fluctuate.

Some people may experience side effects such as nausea, feeling lightheaded, and making sudden involuntary movements.

2. Carbidopa-levodopa infusion: In 2015, the FDA approved Duopa, which is a combination of carbidopa and levodopa in a gel form which is administered via a feeding tube into the small intestine.

Duopa is generally given to patients with advanced Parkinson’s disease whose response to carbidopa-levodopa is varied. The drug is infused continuously so the level of the drugs remains constant.

The risks associated with Duopa are infections at the site of the feeding tube and the tube falling out.

3. Dopamine agonists: Dopamine agonist mimic the effects of dopamine in the brain. They are generally not as effective as levodopa but the effects last longer and they can be used in conjunction with levodopa to counter any fluctuation in efficiency.

These medications can be administered through a patch, oral medications or as an injection. The side effects are also nausea and lightheadedness, but may also cause drowsiness, hallucinations and compulsive behaviors such as gambling, overeating, and hypersexuality — which will need to be addressed by a doctor.

MORE: Find out about the four possible causes of Parkinson’s disease here.

4. MAO-B inhinitors: Medications such as selegiline and rasagiline help to prevent dopamine breaking down in the brain by releasing monoamine oxidase B (MAO-B) enzymes.

Generally, these types of medications should not be taken in conjunction with certain narcotics or antidepressants as occasionally patients will suffer from severe reactions. Side effects of MAO-B inhibitors include insomnia and nausea and if taken with carbidopa-levodopa they can also cause hallucinations.

5. Catechol-O-methyltransferase (COMT) inhibitors: These types of medications help to prolong the effects of levodopa by blocking brain enzymes that deplete dopamine.

The side effects are the same as taking levodopa, mainly involuntary movements and diarrhea.

6. Anticholinergics: Traditionally, anticholinergics have been used over the years to help combat tremors commonly experienced in Parkinson’s disease patients.

However, side effects such as confusion, hallucinations, memory loss, constipation, and urination problems are often more troublesome than the tremors.

MORE: Seven ways to make your home safer for people with Parkinson’s disease

7. Amantadine: Amantadine can be prescribed to patients in the early stages of Parkinson’s to offer relief from their symptoms. In can also be taken in combination with carbidopa-levodopa in the later stages of the disease to help control side effects such as involuntary movements.

8. Deep brain stimulation: Most regularly used in advanced cases of Parkinson’s disease for patients who no longer respond to levodopa, deep brain stimulation involves the insertion of electrodes in the brain which are connected to a generator implanted in the chest area. The electrical pulses sent from the generator to the electrodes can reduce the symptoms of Parkinson’s disease.

The surgery carries serious risks such as brain hemorrhage, stroke, and infection. In addition, patients may need the equipment adjusting or parts replaced which involves more surgery.

MORE: Discover seven ways to help you self-manage Parkinson’s disease

 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 other 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.

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Excessive Calcium Levels in Brain May Play Role in Parkinson’s Disease

calcium

Excessive levels of calcium in the brain may trigger the formation of toxic protein clumps that typify Parkinson’s disease. This finding could be a new treatment target for researchers working to understand how and why people develop the neurodegenerative disease.

The research, “C-terminal calcium binding of α-synuclein modulates synaptic vesicle interaction,” was published in the journal Nature Communications.

Parkinson’s patients typically exhibit Lewy bodies — protein clumps made of alpha-synuclein proteins that aggregate and form filament-like structures — in the brain.

The physiological function of alpha-synuclein has been the focus of intensive research, though with uncertain results. Studies have indicated it is involved in neuronal communication, but its precise mechanisms of action remain unknown.

“Alpha-synuclein is a very small protein with very little structure, and it needs to interact with other proteins or structures in order to become functional, which has made it difficult to study,” the study’s senior author, Gabriele Kaminski Schierle, PhD, said in a press release. Schierle is in the Department of Chemical Engineering and Biotechnology at the University of Cambridge,

The team used super-resolution microscopy methodologies to study small, isolated synaptic vesicles located in the tips of nerve cells that store the neurotransmitters that are released upon communication between neurons.

Calcium plays a key role in the regulation of nerve cell communication. The researchers observed that following an increase in calcium levels, alpha-synuclein binds to synaptic vesicles, causing the vesicles to come together.

“This is the first time we’ve seen that calcium influences the way alpha-synuclein interacts with synaptic vesicles,” said Janin Lautenschlager, PhD, the study’s first author. “We think that alpha-synuclein is almost like a calcium sensor. In the presence of calcium, it changes its structure and how it interacts with its environment, which is likely very important for its normal function.”

There needs to be a physiological balance of calcium and alpha-synuclein in nerve cells. If this balance is disrupted, “the balance is tipped and aggregation begins, leading to Parkinson’s disease,” said co-first author Amberley Stephens, PhD.

The factors that may cause this imbalance include a genetic doubling of alpha-synuclein levels, age-related slowing of protein breakdown, elevation of calcium levels in neurons sensitive to Parkinson’s, and/or a lack of calcium buffering capacity in these neurons.

“Understanding the … role of alpha-synuclein in physiological or pathological processes may impact strongly on the development of new therapeutics for [Parkinson’s]” the investigators wrote.

Ongoing clinical trials in Parkinson’s patients are evaluating the clinical benefit of antibodies that target the calcium-sensitive region of alpha-synuclein (NCT03100149, currently recruiting up to 300 participants), and of calcium channel blockers (NCT02168842), which are used in treating heart diseases.

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Defects in Mitochondria May Contribute to Parkinson’s Disease, Study Suggests

mitochondria

Mutations in mitochondria, which result in a shortage of energy, may be an underlying cause of movement difficulties associated with Parkinson’s disease (PD), a study suggests.

The study, “PINK1 Phosphorylates MIC60/Mitofilin to Control Structural Plasticity of Mitochondrial Crista Junctions,” was published in the journal Molecular Cell.

Parkinson’s disease is caused by the death or malfunction of dopaminergic neurons, which regulate muscle movement and coordination. To do their job, these nerve cells require large amounts of energy, provided by mitochondria.

Mitochondria need to move around the cell to reach the place where they are needed to provide the necessary energy to dopaminergic neurons. Inability of mitochondria to do so can have severe consequences.

Researchers have now discovered that an enzyme (protein) called PINK1 plays a key role in mitochondrial function. This enzyme works to stabilize a mitochondrial protein, called MIC60, which is vital for energy production.

To mimic Parkinson’s, the team used fruit flies, whose brains work similarly to humans to control voluntary movement. They tested how several mutations in the PINK1 gene — known to be a cause of familial forms of early-onset Parkinson’s — affected mitochondria function in the flies.

Several of these mutations were highly damaging to the flies, leading to death in adult flies and significantly impairing crawling ability at early developmental stages.

In flies genetically engineered to lack PINK1, reintroducing MIC60 expression restored mitochondria structure and energy production, correcting the flies’ behavioral defects and halting the death of dopaminergic neurons.

“We found that PINK1 is required only in highly energetic regions of the cells,” Xinnan Wang, MD, the study’s lead author and a Stanford neuroscientist, said in a press release.

“This supports the theory that Parkinson’s disease involves local energy shortages inside cells due to mitochochondrial malfunction — and it indicates that targeting mitochondria may have great potential for exploring new therapeutic interventions in Parkinson’s,” she said.

Future research is necessary to discover if mitochondrial structure impairment and function exists in Parkinson’s disease patients and whether it contributes to disease progression.

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Blood Caffeine Levels May Help Diagnose Early Parkinson’s Disease, Study Reports

Caffeine as diagnostic tool

Parkinson’s patients have lower blood levels of caffeine and its byproducts after consuming the stimulant, suggesting that caffeine could be used as a biomarker for diagnosing the disease.

The findings appeared in the study “Serum caffeine and metabolites are reliable biomarkers of early Parkinson disease,” published in the journal Neurology.

Caffeine is an organic molecule that, when consumed through coffee or tea, can stimulate the central nervous system.

There is evidence that daily caffeine consumption reduces the risk of developing Parkinson’s both in men and in women who are not taking hormone replacement therapy.

In addition, caffeine and two of its metabolites — byproducts produced in the body —  reduce nerve cell death in the brain’s substantia nigra region, mice studies have shown. The substania nigra is the main brain area that Parkinson’s affects.

The researchers studied 108 Parkinson’s patients — 58 men and 50 women — and 31 healthy controls. The team also checked 67 other Parkinson’s patients — 33 men and 34 women — and 51 controls for mutations of caffeine-associated genes.

Participants drank between zero and five cups of coffee a day, except for one, who drank more than six.

Parkinson’s patients had lower blood serum levels of caffeine and nine of its metabolites — including the main byproducts theophylline, theobromine, and paraxanthine — than controls, researchers said. This was true regardless of the stage of patients’ disease and how much caffeine they were consuming.

Another finding was caffeine levels in patients with movement complications were lower than in those without.

Even though the findings showed a relation between caffeine serum levels and Parkinson’s, there was no significant association between the severity of the disease and the concentration of caffeine-related substances. There was also no significant difference in serum levels between men and women with Parkinson’s.

Importantly, researchers found no differences in caffeine-related gene mutations between patients and controls. They looked at genes involved in caffeine metabolism or that encoded the caffeine adenosine 2A receptor.

The results prompted the team to conclude that “caffeine metabolite profiles may be reliable diagnostic biomarkers for early Parkinson’s disease.”

Researchers acknowledged that the study had limitations. They noted that it “was conducted at a single university hospital” and that few participants had severe cases of Parkinson’s. The team excluded patients with a history of pneumonia or cancer.

In addition, any medications that participants were taking to deal with their Parkinson’s disease could have influenced their caffeine metabolism, the researchers said.

Nonetheless, the findings suggested that “lower levels of caffeine and caffeine metabolite profiles are promising diagnostic biomarkers” for early Parkinson’s disease, the team wrote.

 

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Patient-on-a-Chip Program Could Benefit Parkinson’s Patients by Pinpointing Effective Treatment

patient-on-a-chip

A new personalized medical strategy that can replicate human biological systems in a small chip may help predict patients’ response to certain treatments based on their genetic makeup.

Called Patient-on-a-Chip, the joint initiative by Cedars-Sinai and Emulate combines Cedars scientists’ expertise in stem cell technology with Emulate’s Human Emulation System, which uses Organs-on-Chips technology to re-create true-to-life biology in a chip roughly the size of an AA battery.

To simulate the complex environment inside the human body, each chip has small channels lined with thousands of living human cells. The chip can receive air and fluids, such as blood, to create a microenvironment that mimics that of the human body.

Using stem cell expertise, researchers can take patients’ blood or skin cells and make any organ cell, such as those of a lung, liver or intestine. Most importantly, these cells retain the unique genetic makeup of the patient.

Several practical clinical applications of this technology can be used to benefit patients. By exposing patients’ cells in Organ-Chips to certain therapies, clinicians can gain more accurate information about how a patient would respond and could then tailor a treatment plan to that individual.

“The medical potential of a Patient-on-a-Chip is extraordinary,” Clive Svendsen, PhD, director of the Cedars-Sinai Board of Governors Regenerative Medicine Institute, said in a press release. “As examples, scientists could use Organs-on-Chips to create a living model of a patient with Parkinson’s disease, amyotrophic lateral sclerosis or Crohn’s disease, a debilitating inflammatory bowel disorder linked to several gene mutations. By flowing drugs through Organ-Chips containing the patient’s own cells and tissue, we could predict which treatment is most beneficial for that patient.”

“By creating a personalized Patient-on-a-Chip, we can really begin to understand how diseases, medicines, chemicals and foods affect an individual’s health,” said Geraldine A. Hamilton, PhD, president and chief scientific officer of Emulate. “The goal of Emulate working with Cedars-Sinai is to advance and qualify the system for new clinical applications and ultimately democratize the technology so that it can have broad impact on patient healthcare.”

A study published last year in the journal Cellular and Molecular Gastroenterology and Hepatology used Emulate’s Organs-on-Chips technology to re-create human intestinal complexity in this small chip.

The study, “Intestine-Chip: A New Model to Understand the Role of the Intestinal Epithelium in IBD by Combining Microengineering Technology and IPSC-Derived Human Intestinal Organoids,” yielded promising data on how organs may respond to different treatments and how the chip could help avoid subjecting the patient to unnecessary and potentially ineffective treatments.

“This project is an important initiative of Cedars-Sinai Precision Health, whose goal is to drive the development of the newest technology and best research, coupled with the finest clinical practice, to rapidly enable a new era of personalized health,” said Shlomo Melmed, MB, ChB, executive vice president of academic affairs and dean of the medical faculty at Cedars-Sinai.

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Hope Is Medicine

hope, Parkinson's hand-grip test

Sherri Journeying Through

In a conference I attended on Parkinson’s disease a few years back, one of the speakers stated, “Hope is medicine.” In many ways, that is so true. Fyodor Dostoevsky said, “To live without hope is to cease to live.” As a Parkinson’s patient, it may be hard to see, find, or feel hope.

Depression can be one of the first overlooked symptoms while Parkinson’s is making its mark in your life. By the time of diagnosis, you may feel like your whole world has caved in, and diagnosis is like a thousand-ton weight that has just landed on top of you as you lie there in a cave of grief.

One of the hardest things for us to talk about, much less deal with as a people in general, is depression. The difficulty of dealing with it only increases when you have a condition like PD, which can lend itself to making depression a star player. It can take a toll on the relationship between the patient and the caregiver, especially if patients neglect or forget to take “happy pills.” It is my firm belief that if we are not taking care of ourselves emotionally and mentally, it will be a struggle to care for ourselves physically. When our mind is not functioning well, we tend to look at our disease with a somewhat distorted vision, making it even harder than it already is to handle. Often, the distorted view only continues our mental downward spiral.

To those struggling to find anything good in this life with Parkinson’s disease: Are you struggling with an outlook of despair and hopelessness? If so, do you think you may be someone who could benefit from help through an antidepressant? This is nothing to be ashamed of, for having PD is real and so is the depression that clings to it. I have told my husband (my caregiver) that he has my permission to ask (when I feel like giving up in life) whether I’ve missed a dose of my meds. I can, within two missed doses, go from having a good day to wanting it all to end. It’s extremely hard, if not impossible, to care for yourself when your desire to keep going is all but gone. But when that desire to live your life to the fullest in spite of PD is there and healthy, this life can be a wonderful thing.

How can a life with Parkinson’s disease be a wonderful thing? As with any disease, it can make you think twice about your view of life. Your life, in particular. Where you may have once thought of yourself as insignificant, worthless, etc., you now (whether you realize it or not) have found that you are of value. Why else would you seek out a doctor’s care? A support group? Because you matter. You may not have worked through the whys or the hows but somewhere, consciously or not, you have realized that your life means something.

Because your life matters. Your quality of life should matter to the fullest extent of which you are capable.

For example, if you can offer some time to one less fortunate — like reading to a hospital patient or listening to a housebound vet tell of his adventures — do it. Doing activities like this can often remind us that things could be worse, and it always feels good to be able to help another.

If you can sing, sing. It’s good for the heart and especially for those with PD — good for the voice.

If you love to do artsy things, don’t stop because of PD. If you have to change to a different art form, change. Just don’t quit.

Walk, if you can. This is good for the muscles, good for your heart, good for the spirit. If only intentionally around the house, walk.

Talk to someone. When we feel like a burden, we can often shut down. This is when I find it hardest to open up, and when I find it most needful to do. Talk to someone. Let them remind you of the truth — you do matter. They’ll remind you that you are here for a reason and gently ask, “By the way, did you take your happy pill today?”

Living with Parkinson’s disease is hard. It’s a day-to-day battle of pain, a fight for control, and an acceptance for the unwanted. It’s learning how to live a new normal while everyone else continues with the familiar. It’s learning to realize you matter and that there’s a reason you were chosen to carry this load, to walk this path. So, while on this journey they call Parkinson’s disease, take care of you. Take good care of you. And don’t forget to take your meds.

“If you’re reading this…
Congratulations, you’re alive.
If that’s not something to smile about,
then I don’t know what is.”
–Chad Sugg, “Monsters Under Your Head

***

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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7 Hand Exercises to Help People With Parkinson’s Disease

In this video from Invigorate Physical Therapy and Wellness, a physical therapist named Madi demonstrates some simple hand and wrist exercises that may be useful for people suffering from Parkinson’s disease.

MORE: Boxing classes prove a big hit with Parkinson’s disease patients

The hand and wrist exercises are designed to help Parkinson’s disease patients with fine motor skills like handwriting and dressing, as well as improving flexibility and dexterity. Madi advises that people do the exercises once a day for a period of two weeks to see if they see any improvement in their hand and wrist strength and dexterity. She also recommends patients try to write before and after completing the exercises to see if they notice a difference.

To help warm your hands up for the day ahead, Madi suggests doing the exercises first thing in the morning, before breakfast.

MORE: Three causes of psychosis in Parkinson’s disease

Parkinsons’s News Today is strictly a news and information website about the disease. It does not provide medical advice, diagnosis or treatment. This content is not intended to be a substitute for professional medical advice, diagnosis, or treatment. Always seek the advice of your physician or another qualified health provider with any questions you may have regarding a medical condition. Never disregard professional medical advice or delay in seeking it because of something you have read on this website.

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Chan Zuckerberg Initiative Calls for Parkinson’s Research Proposals

Facebook's Mark Zuckerberg

The Chan Zuckerberg Initiative is accepting funding applications from researchers who want to do basic science projects on neurodegeneration.

The goal is to increase scientists’ understanding of diseases such as Parkinson’s and Alzheimer’s and attract new talent and ideas.

Grant recipients will become part of the CZI Neurodegeneration Challenge Network, an interdisciplinary collaboration aimed at increasing understanding of the biology that underlies neurodegenerative disorders.

Scientists can apply for two types of funding. One is an CZI Ben Barres Early Career Acceleration Award for researchers who are in the early stages of their work. The other is a CZI Collaborative Science Award. It involves an interdisciplinary collaboration that includes a physician.

Facebook founder Mark Zuckerberg and his wife, Priscilla Chan, started the initiative in 2016. The overarching goal is to cure all diseases before the end of the century.

The program’s focus has been basic research, which can be difficult to obtain funds for because of the long road between laboratory experiments and approval of therapies that arise from them.

Another reason for the basic research focus is that federal spending for such projects has leveled out, according to data from 2015. Federal sources provide less than half of all funding for basic research, compared with 70 percent in the early 1970s.

Scientists have done a lot of research on neurodegenerative diseases in the past several decades. But they need to know a lot more about their underlying biology before they can develop cures.

In Parkinson’s disease, for example, they still do not know why cells that produce dopamine die in a brain region called substantia nigra — and how they die.

The development of treatments for neurodegenerative disorders has led to many complications and a lot of disappointment. In January, Pfizer said it would terminate its research into Parkinson’s and Alzheimer’s after years of unsuccessful results. And in February Merck announced the discontinuation of a Phase 3 clinical trial on an Alzheimer’s treatment, presumably due to lack of effectiveness.

The Neurodegeneration Challenge Network is bringing together outstanding scientists from different disciplines in hopes of shedding light on the basic mechanisms underlying neurodegeneration.

In calling for applications, the Chan Zuckerberg Initiative notes that treatment development efforts “have focused on a relatively narrow set of ideas.” It said it hopes for approaches that reflect a “greater appreciation that these diseases may share common genes, pathways and cellular mechanisms.”

In addition to projects investigating disease mechanisms, it would consider funding the development of animal models that can better mimic neurodegenerative diseases in humans, and projects dealing with non-nerve cells sources of neurodegenerative diseases, such as the immune system.

 

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