Is Parkinson’s an Autoimmune Disease?

This is a new, and likely controversial, idea in Parkinson’s disease; but if true, it could lead to new ways to prevent neuronal death in Parkinson’s that resemble treatments for autoimmune diseases,” said the study’s senior author, David Sulzer, PhD, professor of neurobiology in the departments of psychiatry, neurology, and pharmacology at Columbia University College of Physicians & Surgeons.

The new hypothesis about Parkinson’s emerges from other findings in the study that overturn a deep-seated assumption about neurons and the immune system.

For decades, neurobiologists have thought that neurons are protected from attacks from the immune system, in part, because they do not display antigens on their cell surfaces. Most cells, if infected by virus or bacteria, will display bits of the microbe (antigens) on their outer surface. When the immune system recognizes the foreign antigens, T cells attack and kill the cells. Because scientists thought that neurons did not display antigens, they also thought that the neurons were exempt from T-cell attacks.

“That idea made sense because, except in rare circumstances, our brains cannot make new neurons to replenish ones killed by the immune system,” Dr. Sulzer says. “But, unexpectedly, we found that some types of neurons can display antigens.”

Cells display antigens with special proteins called MHCs. Using postmortem brain tissue donated to the Columbia Brain Bank by healthy donors, Dr. Sulzer and his postdoc Carolina Cebrián, PhD, first noticed—to their surprise—that MHC-1 proteins were present in two types of neurons. These two types of neurons—one of which is dopamine neurons in a brain region called the substantia nigra—degenerate during Parkinson’s disease.

To see if living neurons use MHC-1 to display antigens (and not for some other purpose), Drs. Sulzer and Cebrián conducted in vitro experiments with mouse neurons and human neurons created from embryonic stem cells. The studies showed that under certain circumstances—including conditions known to occur in Parkinson’s—the neurons use MHC-1 to display antigens. Among the different types of neurons tested, the two types affected in Parkinson’s were far more responsive than other neurons to signals that triggered antigen display.

The researchers then confirmed that T cells recognized and attacked neurons displaying specific antigens.

The results raise the possibility that Parkinson’s is partly an autoimmune disease, Dr. Sulzer says, but more research is needed to confirm the idea.

“Right now, we’ve showed that certain neurons display antigens and that T cells can recognize these antigens and kill neurons,” Dr. Sulzer says, “but we still need to determine whether this is actually happening in people. We need to show that there are certain T cells in Parkinson’s patients that can attack their neurons.”

If the immune system does kill neurons in Parkinson’s disease, Dr. Sulzer cautions that it is not the only thing going awry in the disease. “This idea may explain the final step,” he says. “We don’t know if preventing the death of neurons at this point will leave people with sick cells and no change in their symptoms, or not.”


Neurodegeneration’s Spread

Aggregates of the Huntington’s disease-associated protein, huntingtin, can spread among neurons, according to a study published last month  in Nature Neuroscience, giving credence, experts suggest, to the idea that the propagation of mutant proteins may be a unifying feature of neurodegenerative diseases.

Huntington’s disease, a progressive neurodegenerative disorder that impairs both movement and cognition, is caused by dominant mutations in the huntingtin gene that lead to abnormally long stretches of the amino acid glutamine in the huntingtin protein. These proteins tend to clump in affected neurons, although whether the aggregates are a cause of neurodegeneration or perhaps some kind of cellular response to the mutant protein is still a matter of debate.

The huntingtin gene is expressed throughout the nervous system, so it is hard to tell whether huntingtin aggregates originate within the cells in which they are observed.

To answer this question, researchers from the Novartis Institutes for Biomedical Research in Basel, Switzerland, and their academic colleagues introduced neurons with the wild-type huntingtin gene into mutant brain tissue—both in cell culture and in a mouse model. After several weeks, they observed that aggregates of mutant huntingtin protein had appeared in the wild-type neurons, indicating that the protein from the mutant neurons had spread.

“This paper reports for the first time that mutant huntingtin can spread between neurons,” lead author F. Paolo Di Giorgio, who studies Huntington’s and other neurodegenerative diseases at the Novartis Institutes, told The Scientist.

Neurodegenerative diseases including Parkinson’s, Alzheimer’s, amyotrophic lateral sclerosis (ALS), and frontotemporal lobar degeneration have been shown to involve the propagation of aggregate pathology from cell to cell. Evidence is mounting that neurodegenerative diseases share mechanisms with prion diseases—exemplified by mad cow disease and its human counterpart, Creutzfeldt-Jakob disease, in which misfolded, deleterious proteins propagate over long distances and cause other molecules to misfold.

“This is the first time that diseases involving what are called polyglutamine-expanded proteins have been found to involve a process of transneuronal propagation,” said Albert La Spada, who studies neurodegenerative disease at the University of California, San Diego, School of Medicine and penned a companion article about the study but was not involved in the work. Polyglutamine expansion is a feature of eight neurodegenerative diseases, including Huntington’s, La Spada said. “That’s significant because it extends the scope of this mechanism more broadly across potentially all neurodegenerative diseases. That’s what makes this study particularly exciting.”

To see if huntingtin aggregates could propagate, the researchers first grew human embryonic stem cells alongside brain slices from either mice with a Huntington’s-like disease or wild-type mice. The stem cells differentiated into neurons and formed connections with the mutant neurons of the brain slices.  By six weeks of this co-culture, the introduced wild-type neurons exhibited mutant huntingtin aggregates. They also had shorter and fewer appendages than did neurons co-cultured with wild-type brain slices. Further, introduced neurons that exhibited huntingtin aggregates had significantly narrower cell bodies and fewer projections than those that did not.

“Cells that bear these aggregates show abnormal pathology that is more pronounced [with] respect to cells that don’t bear the aggregates,” said Di Giorgio, “so it seems that when the neurons uptake mutant huntingtin—wild-type neurons that don’t carry any mutation—they will start to show signs of cellular atrophy.”

Huntington’s disease typically begins in the striatum, a brain region involved in movement control, and progresses to the cortex. To examine the way Huntington’s disease might affect this neuronal pathway, the researchers co-cultured striatal and cortical brain slices from wild-type and mutant mice. They found that when mutant cortical neurons and wild-type striatal brain slices were cultured together, functional neuronal connections formed between the brain slices, and mutant huntingtin spread to the wild-type neurons.

When researchers tried the reverse approach—linking mutant striatum and wild-type cortex—the two regions did not form neuronal connections, suggesting that mutant huntingtin within the striatum could disrupt corticostriatal connections.

To explore the corticostriatal pathway in vivo, the researchers used a virus to introduce the polyglutamine-repeat-encoding part of the huntingtin gene into the cortical neurons of wild-type mice. The neurons that were infected with the virus developed aggregates as expected, as did the striatal neurons with which the infected cells made connections.

Finally, in order to probe the mechanism of mutant huntingtin spreading, the researchers returned to their original experimental setup—co-cultures of wild-type human neurons and mutant mouse brain slices—and inhibited the synaptic vesicle pathway using botulinum toxin. Blocking the synaptic transmission reduced the spread of the huntingtin aggregates.  

Taken together, these results lend support to the idea that Huntington’s disease shares features with other neurodegenerative diseases, and with prion diseases.

“If neurodegenerative diseases have a unifying feature,” neurobehavioral geneticist X. William Yang from the University of California, Los Angeles, told The Scientist in an e-mail, “then understand[ing] the mechanisms or developing therapies against such common features may have more general implications/utility for all such disorders.” 

“If spreading occurs and drives disease progression, then blocking the spreading process could be a viable treatment approach,” added La Spada. “If the spreading process occurs extracellularly … then immunizing patients against a disease protein could be explored as a therapy.”


Tuning the brain

For Frank Donobedian, sitting still is a challenge. But on this day in early January, he has been asked to do just that for three minutes. Perched on a chair in a laboratory at Stanford University in California, he presses his hands to his sides, plants his feet on the floor and tries with limited success to lock down the trembling in his limbs — a symptom of his Parkinson’s disease. Only after the full 180 seconds does he relax.

Other requests follow: stand still, lie still on the floor, walk across the room. Each poses a similar struggle, and all are watched closely by Helen Bronte-Stewart, the neuroscientist who runs the lab.

“You’re making history,” she reassures her patient.

“Everybody keeps saying that,” replies the 73-year-old Donobedian, a retired schoolteacher, with a laugh. “But I’m not doing anything.”

“Well, your brain is,” says Bronte-Stewart.

Like thousands of people with Parkinson’s before him, Donobedian is being treated with deep brain stimulation (DBS), in which an implant quiets his tremors by sending pulses of electricity into motor areas of his brain. Last October, a team of surgeons at Stanford threaded the device’s two thin wires, each with four electrode contacts, through his cortex into a deep-seated brain region known as the subthalamic nucleus (STN).

But Donobedian’s particular device is something new. Released to researchers in August 2013 by Medtronic, a health-technology firm in Minneapolis, Minnesota, it is among the first of an advanced generation of neurostimulators that not only send electricity into the brain, but can also read out neural signals generated by it. On this day, Bronte-Stewart and her team have temporarily turned off the stimulating current and are using some of the device’s eight electrical contacts to record abnormal neural patterns that might correlate with the tremors, slowness of movement and freezing that are hallmarks of Parkinson’s disease.

Until now, such data have been accessible only when a patient’s brain is exposed briefly during surgery. But being able to make long-term neural recordings from human patients may become increasingly important — especially because researchers are experimenting with using DBS as a treatment for many other neurological conditions, including depression, obsessive–compulsive disorder and Tourette’s syndrome. The networks involved in such disorders are even less well understood than those involved in Parkinson’s disease, says Helen Mayberg, a neurologist at Emory University in Atlanta, Georgia. Devices such as Donobedian’s could change that, allowing scientists to start to understand just how unhealthy neural networks misfire in different diseases, and what DBS actually does to the brain. “Every disease will be different and one size won’t fit all,” Mayberg says. “The new technology is going to enable progress exponentially.”

Eventually, adds Bronte-Stewart, engineers could use the new-found knowledge about brain networks to build even more-advanced brain implants — devices that could interpret the neural signals they record, monitor their own effectiveness and generate personalized treatments.

“This is such an exciting time,” she says. “This is the first time we’re really getting a window into the brain.”

'Black box' beginnings

The roots of DBS reach back to the 1960s, when Parkinson’s disease was commonly treated with surgery to remove or destroy certain brain regions. To pinpoint which areas to target in each patient, some neurosurgeons began to experiment with electrical stimulation. They discovered that the delivery of rapid pulses to the basal ganglia — a cluster of structures including the STN — could markedly reduce the patient’s tremors. By the late 1980s, long-term brain stimulation started to emerge as an alternative treatment to surgery1. DBS has since been approved for the treatment of Parkinson’s and other movement disorders by both the US Food and Drug Administration (FDA) and European regulators, and has been used in more than 100,000 people.

The biological mechanism underlying DBS remains mysterious, and is a subject of controversy. “We’ve been guessing a lot over the last decade or two,” says Michael Okun, a neuroscientist at the University of Florida in Gainesville. “It would be premature for anyone to claim they know exactly how the therapy works.”

There are some clues, however. For example, DBS is not thought to mimic any natural signals in the brain. The high-frequency pulses — delivered at 130–180 times per second for Parkinson’s disease — exceed the 1–100-hertz frequency range of most natural neural communications. Furthermore, with each 60–90-microsecond burst, DBS typically delivers several orders of magnitude more current than any neuron or groups of neurons can produce.

And it does not seem to produce permanent changes in the brain, at least not when applied to Parkinson’s disease, currently one of the most common targets of the technology. Turning on the current can produce immediate relief from symptoms such as tremor and rigidity. But in many people, symptoms return seconds or minutes after the device is turned off, or the battery runs out — which happens every 3–5 years. Nor does the therapy halt the progressive neurodegeneration associated with the disease; in the long run, patients will typically succumb to symptoms that are not well treated by DBS, such as cognitive deterioration.

From the evidence gleaned so far, researchers suspect that DBS does more than affect neural tissue at the site of the electrodes: it somehow disrupts pathological signals that reverberate through multiple brain regions, corrupting their communications.

That theory meshes with the emerging view that Parkinson’s disease, as well as depression and many other neuropsychiatric conditions are best understood as network dysfunctions. “That’s a really important realization that has caught on in the last five years,” says Cameron McIntyre, a biomedical engineer at Case Western Reserve University in Cleveland, Ohio. Indeed, it has helped to launch two major neuroscience efforts in the past year: the US Brain Research through Advancing Innovative Neurotechnologies (BRAIN) Initiative, and the European Union’s Human Brain Project.

The primary target of DBS for Parkinson’s disease, for example — the STN — sits in the middle of a highly interconnected brain network that helps an individual to control his or her motions. There is some evidence that as Parkinson’s destroys neurons in the basal ganglia, the activity of groups of cells in the STN and across this sensorimotor network becomes abnormally synchronized, locking at certain frequencies. DBS seems to release them from these activity patterns, as do some of the drugs that relieve Parkinson’s symptoms.

Recordings from the new generation of neurostimulators are poised to elucidate these mechanisms, not just for Parkinson’s but also — as DBS applications broaden — for psychiatric conditions. The data could help to resolve concerns about the wisdom of expanding the treatment’s usage. Although the sensorimotor network involved in Parkinson’s disease has been mapped in great detail, says Joseph Fins, a medical ethicist at Weill Cornell Medical College in New York City, much less guidance is available on how best to apply the technology to other disorders. “There has got to be a biological rationale for what you’re intending to do,” he says.

But others argue that controlled testing of DBS in humans need not wait for complete or near-complete understanding of the relevant networks. “As a clinician, that’s not really the important question,” says Benjamin Greenberg, a psychiatrist at Brown University in Providence, Rhode Island. “The real questions are: do these treatments help people? Are they safe?”

Okun adds that, unlike the field of movement disorders, the mechanistic study of neuropsychiatric disorders has been slowed by a lack of realistic animal models. “If we’re going to move forward with some of these human diseases, we are going to have to use humans — in a very careful way, of course,” he says.

Zooming in

Mayberg has been doing just that for more than a decade. In 2005 she published one of the first studies on the use of DBS to alleviate severe, treatment-resistant depression. Since then, she has mainly focused her experiments on a structure known as the subgenual cingulate, in which elevated metabolism has been shown to correlate with the severity of a patient’s depression. She estimates that the use of DBS in this region and elsewhere has successfully eased symptoms in 40–60% of the roughly 150 cases of depression reported on so far. But in recent years, her group has begun to do better by using brain imaging to map the dense web of nerve fibres zigzagging through and around the subgenual cingulate, which connects to regions involved in learning, motivation, appetite and sleep. Combining this information with the effects seen in patients, Mayberg is zeroing in on millimetre-scale differences in electrode placement that can make the difference between success or failure.

Potentially, she says, new implants such as the device being tested by Bronte-Stewart could help her team to do even better, allowing researchers to monitor patients’ condition in real time and fine-tune the stimulation pulses to maximize benefit. “There may be an optimal tuning frequency for a given person, and it may not be the same for everyone,” she says.

Creating personalized DBS treatments is a top priority in this field. Just before Donobedian’s meeting with Bronte-Stewart, his neurologist, Camilla Kilbane of Stanford University, spends half an hour tuning the device’s stimulation settings to address his symptoms.

Using a short-range radio device, she programs a pulse generator implanted in Donobedian’s upper chest. The generator — about half the size of a deck of cards — sends electrical pulses through insulated wires that run under the skin of his neck and scalp, and into his brain. Kilbane has already determined during a previous visit the subset of electrode contacts she wants to tweak, and Donobedian has stopped taking his supplementary Parkinson’s drugs overnight so that Kilbane can cleanly isolate the effects of neurostimulation.

As she drops the voltage and the implant can no longer overcome Donobedian’s tremors, his hands and feet begin to quiver again. Within seconds, the tremors grow and spread, until his arms clap against his sides and his shoes tap the linoleum floor. Kilbane clicks the voltage up again, and Donobedian’s limbs calm down — but then his arms begin to tingle, a common side effect of DBS. At intermediate voltages, his right leg stops shaking, but the other continues to tremble.

“It’s stubborn, that left foot!” remarks Kilbane. She spends another 10 minutes inching the voltage up and down, gradually homing in on an optimal setting. Even after this, Donobedian may need to return in the coming months for further fine-tuning.

“What we have right now for DBS works, but it’s very much the first generation,” says Bronte-Stewart. She and others are using the new recording-capable DBS implants as a stepping stone towards ‘closed-loop’ neurostimulators — devices that can continuously track an individual’s brain activity and automatically optimize settings as needed in real-time. As a first step, the Stanford group is beginning to mine the electrical recordings downloaded wirelessly from the implants in Donobedian and other patients to find patterns that correlate with different Parkinsonian symptoms. They are also looking to see how these patterns might change in the context of different actions, such as sitting, standing and walking — data that could not be obtained with bulky hospital machines. Indeed, Bronte-Stewart says, there may not be just one set of ‘optimal’ stimulation parameters. “We may find out there are different frequency ranges that are better for different functions,” she says.

Smarter stimulation

As scientists collect more data, some manufacturers are already starting to make strides in closed-loop technology. Last November, the FDA approved the first closed-loop, implantable neurostimulator for intractable epilepsy, another disorder attributable to network dysfunction. The device, made by NeuroPace in Mountain View, California, monitors neural networks for the first sign of abnormal activity — which in some patients originates again and again at one or a few ‘epileptic foci’ — then responds with a pulse of electrical current to prevent a seizure. “We use stimulation to disrupt that abnormal activity so that it doesn’t get picked up by the adjacent neurons,” explains Frank Fischer, the company’s chief executive.

But Fischer concedes that, whatever the device might do for epilepsy treatment, the technology is not immediately applicable to other conditions. Epilepsy is a comparatively simple disorder, generally consisting of discrete episodes of abnormal brain activity. By contrast, Parkinson’s disease involves a mishmash of symptoms that rise, fall and morph over time. Researchers are still searching for the relevant neural signatures in Parkinson’s and other diseases, and developing the computational tools required to keep up with changing symptoms.

The first laboratory demonstration of a closed-loop DBS system for Parkinson’s disease was reported last year by experimental neurologist Peter Brown at the University of Oxford, UK, for a group of eight patients. Brown plugged the patients’ DBS implants into an external machine, which triggered stimulation of the STN only when certain abnormal brain rhythms were detected. This selective stimulation improved the symptoms by almost 30% compared with standard DBS treatments, which stimulate the brain at regular intervals.

“It’s far short of being introduced into patients,” says Brown of the bulky experimental system, but the demonstration does provide an important proof that the closed-loop concept could work for Parkinson’s disease.

In an effort to accelerate the move towards closed-loop technology, the US Defense Advanced Research Projects Agency (DARPA) last October announced a 5-year, US$70-million programme to support the development of novel brain stimulators. As part of the BRAIN Initiative, the project aims to foster brain implants to treat conditions such as post-traumatic stress disorder, anxiety and traumatic brain injury. The agency is looking for implantable devices that can monitor and manipulate neural activity not just at one or a few sites at a time, but across entire functional networks of neurons. Accomplishing this goal will require the development of new types of miniaturized sensor, as well as detailed network models of brain function to interpret data streaming in from multiple brain areas, says DARPA programme manager Justin Sanchez.

Some of those models may eventually grow out of data from researchers such as Kendall Lee, a neurosurgeon at the Mayo Clinic in Rochester, Minnesota. At last year’s Society for Neuroscience meeting, he presented a prototype DBS system called Harmoni that can deliver current to one area of the brain while recording electrical and neurochemical responses elsewhere (see Nature; 2013). Because the brain uses both electrical and chemical signals to communicate, explains Kevin Bennet, the lead engineer on the project, monitoring each type of data could provide more complete information about what is going on. The group intends to test Harmoni first in patients with movement disorders. But, ultimately, the scientists hope to extend combined chemical and electrical monitoring to psychiatric disorders. “Those will be the most difficult to treat,” says Bennet. “The symptoms are harder to detect and quantify.”

Bronte-Stewart projects that testing might begin in about five years for the first implantable, closed-loop DBS devices for Parkinson’s disease, with psychiatric applications following close behind. It is not clear whether Donobedian and other current research volunteers could be easily upgraded to those systems; much depends on the precise design of the devices. But even if he does not benefit directly from the data he is generating, Donobedian is glad to participate.

“Somebody had to give to me, to get this far,” he says. “If there’s a chance for me to give something back without too much effort, I’d like to help.”

Today I volunteered selling raffle tickets at the Unity Walk for Parkinson’s disease. I had a really amazing time and even though I just had the world’s longest nap because I was really exhausted and the heat was really bad today, I feel really great having done something for the community. I met a lot of wonderful people and a lot that are suffering from the disease or know a loved one that has/had Parkinson’s; which was really heartbreaking. Even though I still haven’t done my report that’s due at uni tomorrow and I’ll probably skip my lectures tomorrow to make up for it, I’m really happy happy that I got the chance to participate. 

Watch on

Adjusting Brain Circuits- Andrez Lozano Neurosurgeon

Awesome stuff!

My Biggest Fear

Most people are afraid of dying, fire, spiders— the “normal” things.  I guess my fear is relatively normal too, but to me it doesn’t seem rational.  My great-grandmother has Parkinson’s, and so do some other distant relatives.  They never showed the early twenties signs like most patients do, their’s all came in their thirties or later.  Sometimes, my lip will start to twitch, or my hands shake for no reason, and I’m always scared that it’s an early sign.  It’s not really a treatable ailment- they can relieve pressure by using tools on something in the back of your brain, but that’s kind of risky and scary.  Just medicine to help make it a little more bearable.  My fear is that I’m going to have it, and that the real signs won’t show up until I have a child, and then I won’t be able to hold or teach things to him/her.  


A big thank you to my friend, Emily, who put me up to this challenge. Having run cross country and track all through high school, 3.1 miles never seemed like a feat to me— until I took a leisurely four years off. Getting back into race gear was a mind game and a physically confusing. My petty aches and pains aside, we decided to run a race for something more challenging than a leg cramp- Parkinson’s disease. 

Louis’ Run took place in Buttonwood Park in New Bedford, Mass. in commemoration of Louis Xifaras who passed away from the degenerative disease. Loving someone who is also fighting this battle made each incline feel easier. 

Pick something you believe in, and run for your life.


Improper protein digestion in neurons identified as a cause of familial Parkinson’s.

Findings point to potential targets for preventing or treating the neurodegenerative disease

Researchers at Columbia University Medical Center (CUMC), with collaborators at the Albert Einstein College of Medicine of Yeshiva University, have discovered how the most common genetic mutations in familial Parkinson’s disease damage brain cells. The mutations block an intracellular system that normally prevents a protein called alpha-synuclein from reaching toxic levels in dopamine-producing neurons. The findings suggest that interventions aimed at enhancing this digestive system, or preventing its disruption, may prove valuable in the prevention or treatment of Parkinson’s. The study was published March 3 in the online edition of the journal Nature Neuroscience.

Parkinson’s disease is characterized by the formation of Lewy bodies (which are largely composed of alpha-synuclein) in dopamine neurons. In 1997, scientists discovered that a mutation in alpha-synuclein can lead to Lewy body formation. “But alpha-synuclein mutations occur in only a tiny percentage of Parkinson’s patients,” said co-lead author David L. Sulzer, PhD, professor of neurology, pharmacology, and psychiatry at CUMC. “This meant that there must be something else that interfered with alpha-synuclein in people with Parkinson’s.”

Dr. Sulzer and his colleagues suspected that a gene called leucine-rich repeat kinase-2 (LRRK2) might be involved. LRRK2 mutations are the most common mutations to have been linked to Parkinson’s. The current study aimed to determine how these mutations might lead to the accumulation of alpha-synuclein.

“We found that abnormal forms of LRRK2 protein disrupt a critical protein-degradation process in cells called chaperone-mediated autophagy,” said Dr. Sulzer. “One of the proteins affected by this disruption is alpha-synuclein. As this protein starts to accumulate, it becomes toxic to neurons.” Delving deeper, the researchers found that LRRK2 mutations interfere with LAMP-2A, a lysosome membrane receptor that plays a key role in lysosome function.

(Chaperone-mediated autophagy, or CMA, is responsible for transporting old or damaged proteins from the cell body to the lysosomes, where they are digested into amino acids and then recycled. In 2004, Dr. Sulzer and the current paper’s other co-lead author, Ana Maria Cuervo, MD, PhD, professor of developmental & molecular biology, of anatomy & structural biology, and of medicine at Albert Einstein College of Medicine of Yeshiva University, showed that alpha-synuclein is degraded by the CMA pathway.)

“Now that we know this step that may be causing the disease in many patients, we can begin to develop drug treatments or genetic treatments that can enhance the digestion of these disease-triggering proteins, alpha-synuclein and LRRK2, or that remove alpha-synuclein,” said Dr. Sulzer.

While LRRK2 mutations are the most common genetic cause of Parkinson’s, it is too early to tell whether these findings, and therapies that might stem from them, would apply to patients with non-familial Parkinson’s, the more common form of the disease. “Right now, all we can say is that it looks as though we’ve found a fundamental pathway that causes the buildup of alpha-synuclein in people with LRRK2 mutations and links these mutations to a common cause of the disease. We suspect that this pathway may be involved in many other Parkinson’s patients,” said Dr. Sulzer.

The study involved mouse neurons in tissue culture from four different animal models, neurons from the brains of patients with Parkinson’s with LRRK2 mutations, and neurons derived from the skin cells of Parkinson’s patients via induced pluripotent stem (iPS) cell technology. All the lines of research confirmed the researchers’ discovery.

Parkinson's Law Explains Procrastination

Parkinson’s law is the adage that “work expands so as to fill the time available for its completion”. 

Articulated by Cyril Northcote Parkinson as part of the first sentence of a humorous essay published in The Economist in 1955,[1][2] it was reprinted with other essays in the book Parkinson’s Law: The Pursuit of Progress (London, John Murray, 1958). A current form of the law is a mathematical equation describing the rate at which bureaucracies expand over time - bureaucracies are great examples of ‘little work taking forever to complete’. 

A famous corollary is “If you wait until the last minute, it only takes a minute to do”.  In other words, if I have two weeks to do an assignment but I wait until the night before to complete, and I actually do complete it the night before, then the assignment would not have taken me two weeks to complete. Or better yet, if you give me an hour to do a 15 minute task, it will take me an hour. 

People, in general, will use up all resources allotted.  Most do not understand the concept of saving - whether it is time management, money management, or any other type of management. But I don’t consider this procrastination though, it is more passion than procrastination.  Deadlines motivate people more than accountability or responsibility. The line at which you die is a game changer.  Very few people fear accountability but many more people fear penalty.  So I say, insert more deadlines, allow for less time and resources to be wasted. Give only 24-48 hours for an assignment to be turned in, allow only 15 minutes for a task to be completed and then watch how accountable people will be.  

Such freedom with resources is a death trap, an illusion or sorts because people are poor managers.  People are greedy and will ‘use it all up’.  People are renters and not owners; people look for the shortcut instead of enjoying the journey. 

This is a bit pessimistic but I can’t believe that procrastination will ever cease to exist. When completion is the goal, procrastination is fodder for discussion.  Did the task get completed? That is more important - I guess. Everything else is a combination of learned behavior and comfort.


Hip-Hop Wired

Michael J. Fox’s birthday is June 9. Hell, Marty McFly’s birthday is reportedly known to be June 12. Why the tenured actor who famously suffers from Parkison’s Disease is being wished a Happy Birthday across social media is anyone’s guess, but he appears to be victim of a cruel Internet hoax. Naturally the first instinct […]

The post Disrespectful Trolls Slander Michael J. Fox During Birthday Hoax [Photos] appeared first on Hip-Hop Wired.