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I have Parkinson's diseases and thought it would be nice to have a place where the contents of updated news is found in one place. That is why I began this blog.

I copy news articles pertaining to research, news and information for Parkinson's disease, Dementia, the Brain, Depression and Parkinson's with Dystonia. I also post about Fundraising for Parkinson's disease and events. I try to be up-to-date as possible.

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Friday, October 14, 2016

Brain Stimulation for Parkinson’s Patients May Improve Slow, Rigid Movement

OCTOBER 13, 2016 Joana Fernandes, PhD

Treating Parkinson’s disease patients with high-frequency repetitive transcranial magnetic stimulation (rTMS) on both sides of the brain’s motor cortex improves bradykinesia (slow movement) and rigidity, according to a clinical trial analysis presented at the Fourth World Parkinson Congress, in Portland, Ore.
The finding resulted from the analysis of a subset of patients from a the trial called “Magnetic Stimulation for the Treatment of Motor and Mood Symptoms of Parkinson’s Disease (MASTER-PD; NCT01080794).”
“Stimulation of the motor area can help Parkinson’s symptoms, and this can be sustained over time,” said Dr. Alessandro Di Rocco, of the Fresco Institute for Parkinson’s & Movement Disorders at NYU Langone Medical Center in New York City, according to Medscape Medical News. “Knowing which symptoms are helped by TMS may be important to define better the target area.”
The MASTER-PD study included Parkinson’s patients with significant medication-resistant motor problems. Compared to a placebo, high-frequency stimulation of both sides of the brain’s motor cortex improved motor symptoms.
To understand exactly what symptoms were improved by the treatment, the team analyzed a subset of 29 patients from the original study. Those assigned to the TMS group received 10 daily sessions of motor cortex stimulation over both sides of the head (2000 stimuli). Researchers then analyzed scores based on the United Parkinson’s Disease Rating Scale Part III (UPDRS III) that were collected at the beginning of treatment and one month later (the higher the value, the more disease had progressed).
Decreases on the scale correlated with reductions in slow movement and rigidity among patients who received cortex stimulation, compared to the control group. Axial symptoms and tremor scores were not significantly different between the two groups.

Parkinson’s disease risk may triple with depression: Study

By: Dr. Victor Marchione | Brain Function | Friday, October 14, 2016

Parkinson’s disease risk may triple with depression. Study author Albert C. Yang said, “Depression is linked in other studies to illnesses such as cancer and stroke. Our study suggests that depression may also be an independent risk factor for Parkinson’s disease.”
The researchers analyzed medical records of 4,634 people with depression and 18,544 people without depression over the course of 10 years. The researchers also looked at the risk of Parkinson’s disease after excluding those already diagnosed within two to five years of depression diagnosis.
During the follow-up period, 66 people with depression and 97 without depression were diagnosed with Parkinson’s disease. The researchers found that having depression triples the risk of developing Parkinson’s.
Yang concluded, “Many questions remain, including whether depression is an early symptom of Parkinson’s disease rather than an independent risk factor for the disease. Our study also found that depression and older age and having difficult-to-treat depression were significant risk factors as well.”

Depression often remains untreated in many Parkinson’s disease patients

Although depression is a well-known symptom of Parkinson’s disease, it often goes untreated. In fact, it is the most prevalent non-motor symptom of Parkinson’s.
Researcher Danny Bega explained, “We confirmed suspicion that depression is a very common symptom in Parkinson’s disease.  Nearly a quarter of the people in the study reported symptoms consistent with depression. This is important because previous research has determined that depression is a major determinant of overall quality of life.”
The researchers looked at medical records of over 7,000 people with Parkinson’s disease. Among those with the highest levels of depressive symptoms, only one-third were prescribed treatment medications prior to the start of the study, and even fewer were seeing a social worker or mental health specialist.
The researchers then focused on the larger group of patients not receiving treatment for depression. During the follow-up period, less than 10 percent were prescribed antidepressants or referred to a councilor.
Dr. Bega added, “The majority of these patients remained untreated. Still, the physician recognition of depression in this population was actually better than previous reports had suggested.”
“Physicians must be more vigilant about screening patients for depression as part of a routine assessment of Parkinson’s disease, and the effectiveness of different treatments for depression in this population need[s] to be assessed,” he concluded.

Treatment options for patients with Parkinson’s disease and depression

Researchers found that dopamine-replacement therapy could better help treat depression in Parkinson’s disease. Moreover, non-depressed Parkinson’s disease patients benefitted from dopamine-replacement therapy, experiencing an improved cognitive function.
Principal investigator Lee Blonder said, “This was a surprise. It is the opposite of our original hypothesis that both groups of PD [Parkinson’s disease] patients would improve in cognitive performance on dopaminergic medications, and that mood in the depressed PD group would also improve.”
The study included 28 Parkinson’s disease patients – 18 without depression and 10 with depression – and were assessed for cognitive function at baseline.
Due to the small size of the study, the results are only preliminary. Blonder added, “Additional studies are required before these results should be used to alter treatment plans. [But] future research should ultimately focus on investigating treatment options for patients with Parkinson’s and depression to maximize patient function without compromising their mental health.”

New Stem Cell Transplant System for Parkinson’s Disease Improves Cell Survival


Researchers using a new system with real-time imaging to guide transplants of neurons into the brains of non-human primate models with Parkinson’s Disease not only allowed better oversight of the procedure, but also improved cell survival.
The research report, “Real-Time Intraoperative MRI Intracerebral Delivery of Induced Pluripotent Stem Cell-Derived Neurons,” published in an early online release by the journal Cell Transplantation, marks another advance for stem-cell derived neuron transplants in patients.
The transplant involves taking skin cells from a patient and turning them into induced pluripotent stem cells in the lab. Simply, the cells are genetically modified to behave like embryonic stem cells that are able to form all adult cell types, including dopamine producing neurons that can be inserted into the brains of patients.
The approach has posed challenges for Parkinson’s disease. During surgery, cells are not able to survive long at room temperature and they tend to clog the very thin tube tool (cannula) that is used to inject the cells into the brain.
The research team at University of Wisconsin-Madison developed the new system using magnetic resonance imaging (MRI) to guide the transplant of the cells and make the process faster and more accurate. In the study report, the research team described how they upgraded the system to work in real-time, allowing researchers to use the tool not only before, but also during surgery.
The team tested the system in the lab to determine which cannula would be best to use, and worked to reduce the time the cells were in the device before being injected — both crucial aspects in assuring cell survival. The system also permitted researchers to monitor injection pressure to prevent clogging the cannula.
Researchers then tested the system on non-human primates. Brain analyses showed that the neurons survived well after the transplant.
“Cell therapy is the cornerstone of regenerative medicine for neurodegenerative disease,” Paul Sanberg, a distinguished professor at the University of South Florida and co-editor-in-chief for the journal said in a news release. “With the advent of induced pluripotent stem cells, the field has made significant advances.”’s-Disease-Improves-Cell-Survival

Substance with the potential to postpone aging

October 14, 2016

Credit: University of Copenhagen

The coenzyme NAD+ plays a main role in aging processes. In mice and roundworm adding the substance can both extend life and postpone the onset of aging processes. New research conducted at the Center for Healthy Aging and the American National Institute of Health shows that this new knowledge will eventually be able to help patients with Alzheimer's and Parkinson's disease.

As we live longer and longer, a lot of people are occupied with their state of health and, not least, quality of life in old age. Therefore, researchers all over the world are trying to understand aging mechanisms, as this knowledge may eventually help to postpone physical aging and extend life. None of the existing explanations of physical aging are able to explain all the biological aspects of human aging.
Substance Bridges Gap
Previous research has shown that a main process in aging is the capacity of the cells to keep our genes, our DNA, more or less intact. However, changes in the cells' , the mitochondria, also affect aging processes. An international team of researchers from the Center for Healthy Aging at the University of Copenhagen and the National Institute of Health in the United States has shown that the substance NAD+ bridges the gap between two main aging theories - repairs to the DNA and poor functioning mitochondria. The results have just been published in the leading journal Cell Metabolism.
'Our new study shows an age-dependent decrease in the level of NAD+, and this decrease is far greater for organisms with early aging and a lack of DNA repairs. We were surprised to see that adding NAD+ postponed both the aging processes of the cells and extended life in worms and in a mouse model', says Professor Vilhelm Bohr from the Center for Healthy Aging and the National Institute of Health.
The researchers have bred mice and roundworm with the illness Ataxia telangiectasia, A-T, for the purpose of the study. In A-T patients the part of the brain that is responsible for coordination gradually degenerates, DNA repairs are lacking, and they experience other symptoms characteristic of early aging.
Adding NAD+ Postpones Aging
'We know from previous studies that a drop in the level of NAD+ results in metabolism errors, neurodegeneration and aging, but the underlying mechanisms remain unclear to us. Our new study stresses that the substance NAD+ plays a main role both in maintaining the health of the cells' power stations and in their capacity for repairing the genes', says Professor Vilhelm Bohr.
The study also indicates that damage to the DNA can result in poor functioning mitochondria, and that this can lead to increasing neurodegeneration in A-T patients. Adding the substance NAD+ can stop the damage to the mitochondria.
Help for Patients in the Future
Even though the researchers have only examined the effect of the substance on model organisms and not administered the substance to patients, they expect to see the same effect in humans, as the cell repair mechanisms are universal for the cells of all living organisms. Understanding the universal mechanisms at cell level is key to understanding human aging and why we become more susceptible to illness as we grow older. Hopefully, this new knowledge will be able to help postpone physical aging processes and prevent illnesses such as Alzheimer's and Parkinson's disease.
More information: Evandro Fei Fang et al. NAD+ Replenishment Improves Lifespan and Healthspan in Ataxia Telangiectasia Models via Mitophagy and DNA Repair, Cell Metabolism (2016). DOI: 10.1016/j.cmet.2016.09.004
Journal reference: Cell Metabolism

Thursday, October 13, 2016

Untangling a Cause of Memory Loss in Neurodegenerative Diseases

Summary: A new study identifies a possible therapeutic target for memory loss in some neurodegenerative diseases, including Alzheimer’s.

Source: NIH/NINDS.

Sections of brains from normal (left) and tauopathy (right) mice. The dark purple lines in the left image represent the hippocampus, the area most responsible for learning and memory. This structure is almost completely absent in the right image.
CREDIT image is credited to Ashe lab.

NIH-funded mouse study identifies a possible therapeutic target for a family of disorders.
Tauopathies are a group of neurodegenerative disorders, including Alzheimer’s disease that are characterized by the deposition of aggregates of the tau protein inside brain cells. A new study reveals that the cutting of tau by an enzyme called caspase-2 may play a critical role in the disordered brain circuit function that occurs in these diseases. Of interest, the culprit tau fragment identified in this study is actually resistant to forming aggregates, and it causes a disturbance in memory function in animal models before brain cell loss occurs.
In mice genetically engineered to mimic aspects of human tauopathy disorders, the researchers restored some of the learning and memory deficits by blocking caspase-2 activity, which suggests that some of the cognitive loss seen in tauopathies might be reversible. The study was funded by the National Institutes of Health’s National Institute of Neurological Disorders and Stroke (NINDS) and published in the journal Nature Medicine.

“The results of this exciting study suggest that the cognitive loss that occurs in tauopathy may be reversed by blocking the function of caspase-2,” said Roderick A. Corriveau, Ph.D., a program director at NINDS. “This motivates further investigation of caspase-2 as a novel therapeutic target for dementia.”

Using a mouse model of tauopathy that produces a mutated form of human tau protein, researchers correlated memory deficits with the presence of a fragment of the tau protein. The tau fragment, which is produced when caspase-2 cuts the full-length tau protein at a specific location, was also found at higher levels in the brains of Alzheimer’s disease patients compared to healthy individuals of the same age.

While the standard hallmark of tauopathies is the appearance in brain tissue of large tangles of abnormal tau protein, it has recently become less clear whether the tangles of tau are actually causing cognitive decline.

“In the past, many studies focused on the accumulation of tangles and their connection to memory loss,” said Karen H. Ashe, M.D., Ph.D., professor of neurology at the University of Minnesota and senior author of this study, “but the more we learn, the less likely it seems that they are the cause of disease symptoms. The pathological fragment of tau that we have identified resists forming tangles and can instead move freely throughout the cell. Therefore, we decided to look for other mechanisms that could affect synaptic function.”

To do this, Dr. Ashe’s group used fluorescent labeling to track and compare the behavior of normal and mutated tau in cultured neurons from the rat hippocampus, the brain region most associated with learning and memory. Unlike normal tau, both mutated tau and the short fragment produced when caspase-2 cuts tau were primarily found within structures called dendritic spines, where neurons receive inputs from neighboring cells. The overabundance of mutated tau, including the caspase-2-produced fragment, caused disruptions in synaptic function in the spines. The impact on synapses was specific, with no observed effects on the overall structure or survival of the neurons.
“It appears that abnormally processed tau is disrupting the ability of neurons to properly respond to the signals that they receive, producing memory deficits independent of tangle formation,” said Dr. Ashe. “Because this effect is occurring without cell death or a loss of synapses, we have a better chance of intervening in the process and hopefully reversing symptoms of the disease.”
Dr. Ashe and her team are now planning additional experiments to uncover the mechanisms by which abnormally processed mutant tau produces memory deficits.
Funding: The study was supported by the NIH (NS63214 and NS79374) with additional funding provided by the T. and P. Grossman Family Foundation, B. Grossman, and K. Moe.
Source: Carl Wonders – NIH/NINDS
Image Source: image is credited to Ashe lab.
Original Research: Abstract for “Caspase-2 cleavage of tau reversibly impairs memory” by Xiaohui Zhao, Linda A Kotilinek, Benjamin Smith, Chris Hlynialuk, Kathleen Zahs, Martin Ramsden, James Cleary and Karen H Ashe in Nature Medicine. Published online October 10 2016 doi:10.1038/nm.4199

Caspase-2 cleavage of tau reversibly impairs memory
In Alzheimer’s disease (AD) and other tauopathies, the tau protein forms fibrils, which are believed to be neurotoxic. However, fibrillar tau has been dissociated from neuron death and network dysfunction, suggesting the involvement of nonfibrillar species. Here we describe a novel pathological process in which caspase-2 cleavage of tau at Asp314 impairs cognitive and synaptic function in animal and cellular models of tauopathies by promoting the missorting of tau to dendritic spines. The truncation product, Δtau314, resists fibrillation and is present at higher levels in brains from cognitively impaired mice and humans with AD. The expression of tau mutants that resisted caspase-2 cleavage prevented tau from infiltrating spines, dislocating glutamate receptors and impairing synaptic function in cultured neurons, and it prevented memory deficits and neurodegeneration in mice. Decreasing the levels of caspase-2 restored long-term memory in mice that had existing deficits. Our results suggest an overall treatment strategy for re-establishing synaptic function and restoring memory in patients with AD by preventing tau from accumulating in dendritic spines.
“Caspase-2 cleavage of tau reversibly impairs memory” by Xiaohui Zhao, Linda A Kotilinek, Benjamin Smith, Chris Hlynialuk, Kathleen Zahs, Martin Ramsden, James Cleary and Karen H Ashe in Nature Medicine. Published online October 10 2016 doi:10.1038/nm.4199

Dysfunction in Neuronal Transport Mechanism Linked to Alzheimer’s


Summary: A new study confirms a mutation caused dysfunction associated with Alzheimer’s and proposes a new therapeutic target.

Source: UCSD.

This is a colorized scanning electron micrograph of a human induced pluripotent stem cell-derived neuron in culture. image is credited to Thomas Deerinck, National Center for Microscopy and Imaging Research, UC San Diego.

Findings confirm mutation-caused problem but also reveal a new therapeutic target.
Researchers at University of California San Diego School of Medicine have confirmed that mutation-caused dysfunction in a process cells use to transport molecules within the cell plays a previously suspected but underappreciated role in promoting the heritable form of Alzheimer’s disease (AD), but also one that might be remedied with existing therapeutic enzyme inhibitors.

The findings published in the October 11 online issue of Cell Reports.
“Our results further illuminate the complex processes involved in the degradation and decline of neurons, which is, of course, the essential characteristic and cause of AD,” said the study’s senior author Larry Goldstein, PhD, Distinguished Professor in the Departments of Neuroscience and Cellular and Molecular Medicine at UC San Diego School of Medicine and director of both the UC San Diego Stem Cell Program and Sanford Stem Cell Clinical Center at UC San Diego Health. “But beyond that, they point to a new target and therapy for a condition that currently has no proven treatment or cure.”

Alzheimer’s disease is a neurodegenerative disorder characterized by progressive memory loss and cognitive dysfunction. It affects more than 30 million people worldwide, including an estimated 5.4 million Americans. One in 10 persons over the age of 65 has AD; one in three over the age of 85. There are currently no treatments proven to cure or reduce the progression of AD.

Genetically, AD is divided into two groups: the much more common sporadic (sAD) form of the disease in which the underlying primary cause is not known and the rarer familial (fAD) form, produced by inherited genetic mutations. In both forms, the brains of AD patients feature accumulations of protein plaques and neurofibrillary tangles that lead to neuronal impairment and eventual cell death.

The prevailing “amyloid cascade hypothesis” posits that these plaques and tangles are comprised, respectively, of amyloid precursor protein (APP) fragments and tau proteins that fuel cellular stress, neurotoxicity, loss of function and cell death. There has been some evidence, however, of another disease-driver: defects in endocytic trafficking — the process by which cells package large, external molecules into vesicles or membrane-bound sacs for transport into the cell for a variety of reasons or uses.

But previous research focused on non-neuronal cells and did not examine the effects of normal expression levels of AD-related proteins, leaving it unclear to what degree decreased endocytosis and other molecular movement within cells played a causative role.
Goldstein and colleagues analyzed neurons created from induced pluripotent stem cells in which they generated PS1 and APP mutations characteristic of fAD using the emerging genome editing technologies CRISPR and TALEN. In this “disease-in-a-dish” approach, they found that the mutated neurons displayed altered distribution and trafficking of APP and internalized lipoproteins (proteins that combine with or transport fat and other lipids in blood plasma). Specifically, there were elevated levels of APP in the soma or cell body while levels were reduced in the neuronal axons.
In previous work, Goldstein’s team had demonstrated that PS1 and APP mutations impaired the activity of specific cellular enzymes. In the latest work, they found that treating mutated fAD neurons with a beta-secretase inhibitor rescued both endocytosis and transcytosis (molecule movement within a cell) functions.
Co-authors of the study include: co-first authors Grace Woodruff and Sol M. Reyna, and Mariah Dunlap, Rik Van Der Kant, Julia A. Callender, Jessica E. Young, and Elizabeth A. Roberts, all at UC San Diego.
Disclosure: Lawrence S.B. Goldstein has an equity interest in Human Longevity, Inc., a company that may potentially benefit from the research results. He also serves on the company’s Scientific Advisory Board. The terms of this arrangement have been reviewed and approved by the University of California San Diego in accordance with its conflict of interest policies.
Funding: The study was funded by National Institutes of Health, California Institute for Regenerative Medicine, Tina Nova scholarship, ERC Marie Curie International Outgoing Fellowship, Alzheimer’s Netherlands Fellowship NIH/National Institute on Aging.
Source: Scott LaFee – UCSD

Image Source: image is credited to Thomas Deerinck, National Center for Microscopy and Imaging Research, UC San Diego.
Original Research: Full open access research for “Defective Transcytosis of APP and Lipoproteins in Human iPSC-Derived Neurons with Familial Alzheimer’s Disease Mutations” by Grace Woodruff, Sol M. Reyna, Mariah Dunlap, Rik Van Der Kant, Julia A. Callender, Jessica E. Young, Elizabeth A. Roberts, and Lawrence S.B. Goldstein in Cell Reports. Published online October 11 2016 doi:10.1016/j.celrep.2016.09.034


Defective Transcytosis of APP and Lipoproteins in Human iPSC-Derived Neurons with Familial Alzheimer’s Disease Mutations

•FAD mutations impair endocytosis and transcytosis of APP and lipoproteins
•Reduced lipoprotein endocytosis and transcytosis are rescued by β-secretase inhibition

We investigated early phenotypes caused by familial Alzheimer’s disease (fAD) mutations in isogenic human iPSC-derived neurons. Analysis of neurons carrying fAD PS1 or APP mutations introduced using genome editing technology at the endogenous loci revealed that fAD mutant neurons had previously unreported defects in the recycling state of endocytosis and soma-to-axon transcytosis of APP and lipoproteins. The endocytosis reduction could be rescued through treatment with a β-secretase inhibitor. Our data suggest that accumulation of β-CTFs of APP, but not Aβ, slow vesicle formation from an endocytic recycling compartment marked by the transcytotic GTPase Rab11. We confirm previous results that endocytosis is affected in AD and extend these to uncover a neuron-specific defect. Decreased lipoprotein endocytosis and transcytosis to the axon suggest that a neuron-specific impairment in endocytic axonal delivery of lipoproteins and other key materials might compromise synaptic maintenance in fAD.

“Defective Transcytosis of APP and Lipoproteins in Human iPSC-Derived Neurons with Familial Alzheimer’s Disease Mutations” by Grace Woodruff, Sol M. Reyna, Mariah Dunlap, Rik Van Der Kant, Julia A. Callender, Jessica E. Young, Elizabeth A. Roberts, and Lawrence S.B. Goldstein in Cell Reports. Published online October 11 2016 doi:10.1016/j.celrep.2016.09.034

Imaging Biomarker for Parkinson’s Clinical Trials Gains EMA Support

LONDON and TUCSON, Oct. 13, 2016 

The Critical Path Institute (C-Path) — part of the Critical Path for Parkinson’s Consortium (CPP) — and Parkinson’s U.K. have garnered the support of the European Medicines Agency (EMA) for the use of an imaging biomarker that will help researchers conduct new treatment clinical trials for patients diagnosed with early-stage Parkinson’s disease . 

The neuroimaging biomarker dopamine transporter imaging system is used as an exploratory biomarker for the early stages of Parkinson’s. CPP's ultimate goal is to achieve biomarker qualification with EMA and the US Food and Drug Administration (FDA). 

"Parkinson's disease treatments are urgently needed, and shaving off time and cost serves to incentivize companies to invest in more trials,” said CPP's executive director Diane Stephenson. “More shots on goal mean more chances of getting approved drugs past the finish line." 

This, in turn, would ultimately relieve trial sponsors of having to convince the regulators that the biomarkers are reliable and reproducible during clinical trials. 

Dopamine transporter activity, as measured by single-photon emission computed tomography (SPECT) imaging, looks at the expression of dopamine nerve terminal function in the living brain. Low levels of the binding serve as a marker of the loss of dopamine nerve terminals, which is a hallmark of Parkinson’s. Use of the biomarker in the early stages of Parkinson’s will help identify patients who are likely to show clinical progression of motor symptoms.

Embedding biomarkers in clinical trials, with support from regulatory agencies could facilitate their use as both therapeutic and prognostic indicators. "This will all happen more quickly due to the significant progress we are making in sharing data across several major studies,” said Donald Grosset, a professor at the University of Glasgow, where Parkinson's research that is contributing data to CPP is being conducted. "This action from the EMA is certainly good news for the field." 

In 2015, the FDA issued a letter of support for this same biomarker and its application in drug development. These more recent letters of support convey that the FDA and EMA both recognize the potential value of a biomarker and encourage its further evaluation.

Growblox Sciences Announces Patent Application for Treatments of Parkinson’s Disease, Alzheimer’s Disease, Huntington’s Disease and Dementia

October 12, 2016 5:15 pm

Growblox Sciences, Inc. (OTCQB: GBLX) is pleased to announce the filing of the first of several patent applications for life science inventions by its wholly-owned subsidiary, Growblox Life Sciences, LLC. The current provisional patent application covers complex-cannabinoid-containing mixtures capable of enhancing dopamine secretion and protect neurons from the mitochondrial-induced free radical damage that occurs during disease progression in the brains of patients with Parkinson’s disease, Alzheimer’s disease, Lewy Body Dementia, and Huntington’s disease, among others. In an aging population, neurodegeneration associated with these disorders is a growing health burden according to the World Health Organization (2013).
For the past two years, GB Sciences has been working towards the creation of novel, patentable cannabis-based formulations under the leadership of Dr. Andrea Small-Howard, Chief Science Officer of GB Sciences, Inc. “This patent application is the first in a series that were invented based on our novel approach to creating cannabis-based therapies. Unlike many other companies and researchers who try to reduce the natural complexity in the cannabis plant, we embrace it and it informs our therapeutic mixtures,” said Dr. Small-Howard. “Additionally, we test our mixtures in disease systems that include a natural diversity of human cannabis-receptors, not just CB1 and CB2 receptors, which are the only receptors studied by many leading cannabinoid researchers. Our fast and efficient screening system then evaluates the effectiveness of the cannabis-based mixtures containing dozens of individually acting agents in order to make effective therapies for different diseases. We intend to start with Parkinson’s disease because these patients are in great need of an effective therapeutic treatment. One additional benefit is that our Parkinson’s treatment does not contain substantial amounts of the psychoactive compound, delta-9 tetrahydrocannabinol.”
GB Sciences’ CEO, John Poss, said, “Our goal is to help the approximately one million patients in the US and ten million world-wide that are living with Parkinson’s disease through our life science research, and we anticipate being able to use the same research processes to create additional innovative therapeutic options for other underserved patient groups in the coming months. Through our current patent application, GB Sciences is poised to participate in the US biopharmaceutical market for neurological disorders, which is projected to reach $128.6 billion by 2020. While there are many regulatory hurdles in front of us, this opportunity dramatically expands the revenue potential for our company over the next five years.”
About Growblox Sciences, Inc.
Growblox Sciences, Inc. (GBLX) is a diverse vertically integrated cannabis company, focused on cultivation as well as biopharmaceutical research and development. The Company’s goal is creating safe, standardized, pharmaceutical-grade, cannabinoid therapies that target a variety of medical conditions. To learn more about Growblox Sciences, Inc., go to:
Forward-Looking Statements
This press release may contain statements relating to future results or events, which are forward-looking statements. Words such as “expects”, “intends”, “plans”, “may”, “could”, “should”, “anticipates”, “likely”, “believes” and words of similar import may identify forward-looking statements. These statements are not historical facts, but instead represent only the Company’s belief regarding future events, many of which, by their nature, are inherently uncertain and outside of the Company’s control. It is possible that the Company’s actual results and financial condition may differ, possibly materially, from the anticipated results and financial condition indicated in these forward-looking statements. Further, information concerning the Company and its business, including factors that potentially could materially affect the Company’s business and financial and other results, are contained in the Company’s filings with the Securities and Exchange Commission, available at All forward-looking statements included in this press release are made only as of the date of this press release, and we do not undertake any obligation to publicly update or correct any forward-looking statements to reflect events or circumstances that subsequently occur or of which we hereafter become aware.
Note: Although the Company’s research and development activities are not illegal, the production and sale of cannabis products violate federal laws as they presently exist.
Contact Information 
Growblox Sciences, Inc.,  
3550 West Teco Ave., Las Vegas, NV 89118  
866-721-0297, or  
Liz Bianco Publicity Director, liz@gbsciences.com 
Investors: John Poss,

Injectable Wires for Fixing the Brain

  • By Julia Sklar
  • October 13, 2016
    Novel treatments for neurological diseases might be possible with a flexible mesh that can prod individual brain cells.

    These meshes don’t tangle or snag easily, even when bunched together in a cup of water.
    Novel treatments for neurological diseases might be possible with a flexible mesh that can prod individual brain cells.
    The mesh electronics—lines of gold between layers of a polymer—are produced in batches on a silicon wafer. 

    This close-up of the mesh shows a pad in the middle that stimulates neurons. Smaller pads measure their activity.

    In a basement laboratory at Harvard University, a few strands of thin wire mesh are undulating at the bottom of a cup of water, as if in a minuscule ribbon dance. The meshes—about the length of a pen cap—are able to do something unprecedented: once injected into the brain of a living mouse, they can safely stimulate individual neurons and measure the cells’ behavior for more than a year.
    Electronic brain interfaces like these could someday be crucial for people with neurological diseases such as Parkinson’s. The disease causes a group of neurons in one area of the brain to begin dying off, triggering uncontrollable tremors and shakes. Sending targeted electrical jolts to this area can help whip the living neurons back into shape and stop Parkinson’s symptoms. 
    Today people can undergo an electrical treatment called deep brain stimulation. But it has big limitations. It involves implanting rigid, dense electrodes in the brain. That’s far from ideal in such a soft organ: after about four weeks, scar tissue begins to build up. The only way to get the electrodes to work through this tissue is to keep upping the voltage used to excite the neurons. That can be dangerous, and sometimes another surgery is required to replace the implant.
    The device is flexible enough to be injected by a needle. The net-like structure prevents it from disrupting neurons too much once implanted.

    The implanted device connects to a computer, which controls the electric jolts and records the neurons’ behavior.
    Charles Lieber, a Harvard chemist and nanomaterials pioneer, had a different idea: a conductive brain interface that mirrors the fine details of the brain itself. Just as neurons connect with each other in a network that has open spaces where proteins and fluids pass through, the crosshatches in Lieber’s bendable mesh electronics leave room for neurons to fit in, rather than being pushed to the side by a boxy foreign object. “This device effectively blurs the interface between a living system and a non-living system,” says Guosong Hong, a postdoc in Lieber’s lab. 
    The extremely flexible mesh, made of gold wires sandwiched between layers of a polymer, easily coils into a needle so it can be injected rather than implanted, avoiding a more extensive surgery. Part of the mesh sticks out though the brain and a hole in the skull so that it can be wired up to a computer that controls the electric jolts and measures the neurons’ activity. But eventually, Lieber says, the controls and power supply could be implanted in the body, as they are in today’s systems for deep brain stimulation.
    The researchers foresee the mesh having many uses beyond Parkinson’s. It might help treat depression and schizophrenia more precisely than today’s drugs, which bathe the entire brain in chemicals and cause an array of side effects.
    First, though, it needs to be tested in humans. Lieber’s group is partnering with doctors at Massachusetts General Hospital and will soon begin experiments in people with epilepsy.

    High school student working on breakthroughs in Parkinson’s disease detection

    OCTOBER 12, 2016, BY 

    OVERLAND PARK, Kan. -- People concerned about Parkinson’s disease now are participating in an online research project called FacePrint. The objective of it is to develop a simple, early and accurate telemedicine approach to detecting the debilitating nervous system disorder. The creator of FacePrint is a high school student and she’s this week’s FOX 4 Young Achiever.
    “This breaks down the face into different component movements.”
    That’s Erin Smith, this week’s FOX 4 Reaching 4 Excellence Young Achiever, demonstrating FacePrint. This remarkable research system is Erin’s baby. She developed it herself based off of biomarkers she discovered in facial muscle movements in people with and without Parkinson’s disease using facial recognition software and machine learning algorithms.
    “And I get different millisecond-by-millisecond analysis of the movement of each section of the face,” said Erin as the fascinating demonstration progressed. The Michael J. Fox Foundation for Parkinson’s Research found out about Erin’s work and now the organization has FacePrint online to help her gather data from a much larger sample size and achieve her ultimate goal:
    “To provide a very easy, simple and early and accurate telemedicine approach to Parkinson’s disease detection,” said Erin.
    She wants to target that technology especially to primary care physicians and clinics and to developing nations where much of the anticipated increase in Parkinson’s disease cases are expected to be. This junior at Shawnee Mission West High School has been doing impressive science and technology research projects for six years already. She calls herself “perpetually curious” and approaches her painstaking work with uncommon diligence and discipline.
    “It kind of becomes addicting in the sense that you get to one point and then you find out this information but then you want to know what that information means and then you have this idea based off that information and so it’s very perpetual and exciting,” said Erin.
    “Erin takes advantage of every opportunity I give her,” said Brenda Bott, an award-winning science teacher who directs the Shawnee Mission School District’s rigorous and advanced Biotechnology Signature Program. Erin’s done much of her work so far under Bott’s guidance in her classroom at West High.
    “You can’t stop her,” said Bott. “She thinks of something new. She thinks of the details. She records, if you talk to her, she’s writing notes. She is very good at networking. She is exemplary in listening.”
    Erin’s phenomenal science and technology research has put her in the spotlight often already, especially for one still so young. She’s been very active in seeking out and winning high level national and international student competitions that have taken her far and wide demonstrating her projects.
    “I’m always known as the more dramatic presenter,” said Erin with laughter. Erin is a national tournament debater, as well, and she really enjoys using her entertaining speaking skills at major science competitions and conferences like last month’s #BUILTBYGIRLS Future Founder Challenge where she won $10,000 and where can also talk movingly about this field she loves so much.
    “It’s really exhilarating,” said Erin, “because it’s anything that you want to do. The sky’s the limit in terms of what you can think of and then actually being able to have an idea that may seem crazy and then being able to create it into reality. It’s one of the greatest feelings in the world.”
    She’s an innovator out to heal people and keep them healthy.
    “Ultimately I want to create technologies and devices that are used in different clinics throughout the world and then also in primary care physician clinics. And I also am really interested in the divide that is happening with health care. I think that there’s going to be a shift as we see it move a lot more to telemedicine approaches. And so, I want to be the one that starts having health care-related stuff on social media and technology like Snapchat. So bridge these two different trends that we are seeing in health care.”
    She's addicted to discovery and blazing new trails in science and technology.
    Erin also is focused on opening doors for other young people, especially girls, to advance in these STEM studies she loves. She’s founded an organization called KC STEMinists to empower girls through a hands-on approach to computer science and coding.  Go to the online application, or contact Erin at for more information and registration on KC STEMinists.
    You can participate in Erin’s FacePrint research study on Parkinson’s disease in her online survey.
    FOX 4 News is Working 4 You to spotlight outstanding young people and their positive accomplishments. In our weekly report called Reaching 4 Excellence we meet young achievers in subjects like academics, the arts, leadership, community service, volunteerism, career exploration, overcoming obstacles and heroism. Watch for Reaching 4 Excellence every Wednesday on FOX 4 News at 9 p.m. and every Thursday on FOX 4 News at 8 a.m. and noon.