Memorial ride to honour late miner who inspired McIntyre Powder Project

March 9, 2018

 Janice Martell, founder of the McIntyre Powder Project (Supplied photo)

 McIntyre Powder was aluminum, finely ground into powder and administered to underground miners as a preventive measure against silicosis, but was later found to be ineffective.

Janice Martell cried when she learned the Ontario Network of Injured Workers Groups (ONIWG) would hold a memorial cycling ride between Massey and Elliot Lake this May in tribute to her late father, Jim Hobbs.

The veteran miner made that same trek countless times between 1978 and 1990 while working for the area’s underground uranium mines. In retirement, Hobbs was diagnosed with Parkinson’s disease – something his daughter attributes to his exposure to a finely ground aluminum dust known as McIntyre Powder – which eventually took his life in May 2017.

That ONIWG is recognizing the significance of occupational disease on the province’s workforce while honouring her father and other miners impacted by McIntyre Powder exposure is a gesture that touched Martell deeply.

“They’re going to be travelling the same route that he would have had to drive every day to go to work,” Martell said. “So it was just really very meaningful that they would come to our area and honour our mine workers.”

Established in 1991, ONIWG is a non-profit organization with 22 member groups advocating for workers who have been injured or become ill while on the job. The organization’s annual cycling ride aims to raise awareness surrounding the challenges addressing injured workers, in addition to raising funds for its advocacy work. This is the first time the ride will travel to Northern Ontario.

To greet the riders, Martell is planning a welcoming reception on Friday, May 25 and Saturday, May 26 at the Lester B. Pearson Civic Centre in Elliot Lake.

It will also give her a chance to share with the general public the information she’s learned over the last four years through the McIntyre Powder Project, which she started in 2014.

“I’ve discovered a lot of information from my research and from talking to mine workers and their survivors,” Martell said.

“I’ve been hearing their stories for four years and I’ve been trying to get out as much information as I can, but I really haven’t sat down with these mine workers and said, look, this is what was going on; these are the documents; this is what I found.”

First introduced in 1943, McIntyre Powder was created by mine executives who were looking for a way to reduce worker compensation costs associated with silicosis, a lung disease caused by inhaling silica dust. The theory was that if miners inhaled aluminum first, it would coat the lungs, protecting them from silicosis.

Aluminum was ground into a fine dust and miners were mandated to breathe it in while in the mine drys at the start of every shift. Miners were not asked for their consent or warned of any possible side effects.

The practice – something Martell calls “a big, human experiment” – was later debunked as ineffective and it ceased in 1980. But years later, miners who had been exposed began experiencing a range of health issues, including everything from respiratory illness to neurological disease.

Martell believes McIntyre Powder is the direct cause, but because there is no scientific evidence correlating the dust with the range of illnesses, miners filing compensation claims with the Workplace Safety and Insurance Board (WSIB) have routinely been denied.

Martell believes that’s unacceptable, based on what she says is evidence that the provincial and federal governments of the time were “kowtowing” to industry instead of fulfilling their duties to monitor what the mine executives were doing and hold them accountable.

“If we're saying that as a society we need this gold, we need this uranium in order to function in society, in order to drive our economy, then we also need as a society to say, ‘We are going to take care of these mine workers if they are injured,’” Martell said.

“‘We are going to do everything in our power to ensure that they don't get injured, to control for carcinogens like silica dust, like diesel emissions.’”

In January, she ramped up her efforts, filing a Freedom of Information Act request with the WSIB to release the information about its policy denying claims associated with aluminum exposure and neurological disease. In response, the WSIB quoted the cost of accessing that information at $7967.95, and Martell has launched a crowdfunding campaign with GoFundMe to raise the funds.

In just nine days, she had raised $3,740 – nearly half her goal.

Since teaming up with the Occupational Health Clinics for Ontario Workers(OHCOW) on a research project in 2016, Martell said a database of 450 workers has been compiled documenting their work histories and health records. Work is ongoing to find common elements among the cases to pinpoint any links or trends.

OHCOW is additionally conducting a “first review” of cases surrounding six specific respiratory diseases: lung cancer, silicosis, sarcoidosis, chronic obstructive pulmonary disease (COPD), pulmonary fibrosis and asbestosis.

“Those are ones that should, really, be granted WSIB; those are all associated with workplace exposures,” Martell said. “So we're looking at all of those cases that have not already put in a WSIB claim, or whose claim has been denied, and working to getting those claims into WSIB.”

For now, any claims associated with neurological disorders such as Parkinson’s disease, Alzheimer’s or amyotrophic lateral sclerosis (ALS) have been put on hold, as they require more research to determine any links to McIntyre Powder.

It’s disappointing for Martell, whose driving motivation for starting the McIntyre Powder Project was finding an explanation for her dad’s Parkinson’s diagnosis. But that explanation may be getting nearer.

Last year, 11 cases of ALS were discovered in the database of 450 miners, which works out to 2.4 per cent. It’s a compelling number considering the national average is two in 100,000, or 0.002 per cent, according to ALS Canada.

Similarly, OHCOW researchers have found 45 cases of Parkinson’s disease, or 10 per cent of cases, in the registry, while the Canadian average sits around 0.2 per cent.

“I honestly think that’s why OHCOW got their funding, because they can’t explain away the ALS numbers,” Martell said.

https://www.northernontariobusiness.com/industry-news/mining/memorial-ride-to-honour-late-miner-who-inspired-mcintyre-powder-project-856809

Parkinson's

March 9, 2018

Way back in the 1980s, I had the dream job of health and fitness editor at the Los Angeles Times Syndicate. For as long as I can remember, I've been curious about all aspects of health, and that job gave me a reason to read and research publications that focus on how our bodies work. 

Ever since then, I've been collecting books that are first-person stories about coping with accidents, illness or disease. Want to know what it's like to live with a facial deformity? Read "Autobiography of a Face" by Lucy Grealy. Wonder what it's like to experience chemotherapy? Read "Time on Fire" by Evan Handler. Are you curious about paralysis? "Still Me" by Christopher Reeve will answer all your questions.

I could make book recommendations all day, but two books have caught my attention recently because they both deal with Parkinson's disease — in different ways. Back in 2003, Michael J. Fox wrote (by hand on yellow legal pads) one of the finest memoirs I've ever read. "Lucky Man" takes the reader into the world of a young (and very successful) actor who is diagnosed with early-onset Parkinson's and learns how to restructure every single aspect of his life. As of this date, The Michael J. Fox Foundation for Parkinson's Research has raised more than $750 million for research. Against all odds, his career is still alive and well, and fans will be able to watch him on ABC's "Designated Survivor" this spring. 

The other book that made me think about the effects of Parkinson's disease is NPR's Diane Rehm's 2016 memoir "On My Own," which deals with her late husband's struggles and eventual death. Her brilliant and accomplished husband, John Rehm, simply could not cope with the gradual losses that followed his diagnosis, and she also had to find ways to reconstruct her life. 

Parkinson's disease is a neurodegenerative disorder that leads to progressive deterioration of motor function. Life expectancy after diagnosis is about the same as for people without the disease. The stages of Parkinson's are listed below:

—Stage one: Mild symptoms (tremors or swinging arms while walking) occur on one side of the body and do not interfere with daily activities.

—Stage two: Walking becomes more difficult, and both sides of the body are affected. 

—Stage three: Abilities become more compromised, including loss of balance and slowing of movement.

—Stage four: Symptoms become more severe; assistance is required; and the individual can no longer live alone. 

—Stage five: A caregiver is needed for all activities. The individual probably cannot stand or walk, may be bedridden and may have either delusions or hallucinations.

Several institutions — including the Northwestern University's Feinberg School of Medicine and University of Colorado's Anschutz Medical Campus — have begun studying the impact of exercise on individuals recently diagnosed with Parkinson's.

The good news, according to an article in the JAMA Neurology journal, is that intense treadmill exercise tends to slow the progression of the disease. Why? Evidently, high-intensity exercise improves brain vascularity and neuronal blood supply. So, if you have just been diagnosed with Parkinson's (or someone you know has), intense aerobic exercise is well worth considering along with other treatment options. 

Marilyn Murray Willison has had a varied career as a six-time nonfiction author, columnist, motivational speaker and journalist in both the U.K. and the U.S. She is the author of The Self-Empowered Woman blog and the award-winning memoir "One Woman, Four Decades, Eight Wishes." She can be reached at www.marilynwillison.com. To find out more about Marilyn and read her past columns, please visit the Creators Syndicate webpage at www.creators.com.

https://www.creators.com/read/positive-aging/03/18/parkinsons

Sidcup nurse invited to Buckingham Palace

09 March 2018 

Carmen Marchidan, clinical services manager at Bupa Abbotsleigh Mews Care Home, Old Farm Road, will join other front-line nurseat the royal event.

Emblazoned with the golden letterhead of the Queen, the invitation states: “The Master of the house has received Her Majesty’s command to invite Mrs Carmen Marchidan to a reception at Buckingham Palace.”

It also goes on to say that the reception will be in the presence of the Prince of Wales, on the evening of March 14.

Carmen said: “I have no idea who nominated me for this event – it’s such an honour.

“I am very excited to be attending, and to be representing such a great team of staff at Bupa UK.”

Carmen manages the four homes within Abbotsleigh Mews, which cover a range of specialist care needs including dementia, Parkinson’s disease and palliative care.

Her roles in maintaining the homes are extensive - Carmen checks for problems, attends emergency situations, offers her staff support and carries out nurse shifts when necessary,

She first qualified as a nurse more than 30 years ago, and has worked in care homes ever since.

She added: “It’s a very busy role, but it is the job I always dreamed of as a child and I couldn’t see myself ever working in another field.

“I’m very proud to work with so many talented nurses and care professionals.

“Going to the palace definitely isn’t something I ever expected – I’ll have to start practising my curtsey.”

Carmen’s manager, Tracey Cheeseman RGN, general manager at the care home, added: “Carmen is an amazing nurse.

“She is just the kind of person I’d like to be looking after me or anyone I care about.

“She is great fun to work with, is an amazing source of inspiration and a valued support to me and the team, as well as residents and visitors to the home.

“We’re so lucky to have her.”

http://www.bexleytimes.co.uk/news/sidcup-nurse-invited-to-buckingham-palace-1-5426992

Michael J. Fox Foundation Holds Parkinson’s Program at Putnam Hospital Center

By Kathy Welsh -March 9, 2018

Board members Tracy Pollan, Lily Safra and Michael J. Fox at A Funny Thing Happened on the Way to Cure Parkinson's. Photo Getty Images

CARMEL – Celebrated actor Michael J. Fox is known just as much for his starring roles in “Back to the Future” and “Spin City” as he is as a spokesperson and activist for Parkinson’s research.

Fox, who was diagnosed with early-onset Parkinson’s disease in 1991 at age 30, launched the Michael J. Fox Foundation for Parkinson’s Research in 2000 to both find a cure and develop therapies for those living with the neurodegenerative disorder.

The foundation’s advancement officers, Nicole Prisco and Mary McQuillen, will give a presentation at Putnam Hospital Center at 3 p.m., Monday, March 19, in the Michael T. Weber Auditorium, 670 Stoneleigh Ave. They will provide an overview of the foundation, as well as an update on Parkinson’s disease research in the pipeline and information on how people can get involved in online clinical trials.

The program is free and open to the public.

Parkinson’s is a neurodegenerative brain disease that has no cure. The disease damages dopamine-producing cells affecting the brain’s ability to control movements of the human body.

At Putnam Hospital Center, there is a robust Movement Disorders Support Group that meets once a month for families and patients with neurological disorders, including essential tremors, Huntington’s or Parkinson’s disease. The group is led by speech pathologist Jenny Kalanz and physical therapist Kirsi Vera from the hospital’s Rehabilitation Department.

The Movement Disorders Support Group meets from 3 to 4 p.m. the third Monday of each month in the Michael T. Weber conference room 2 at Putnam Hospital Center, 670 Stoneleigh Ave. For more information on the support group, call 845-279-5711 ext. 2483 (TTY 1-800-421-1220).

https://hudsonvalleynewsnetwork.com/2018/03/09/michael-j-fox-foundation-holds-parkinsons-program-putnam-hospital-center/

LRRK2 Gene: A Possible Link between Crohn’s and Parkinson’s Disease

March 9, 2018

In a recent study published in Science Translational Medicine researchers examined the link between gene variants in Crohn’s disease and Parkinson’s disease.

The current treatments available for inflammatory bowel diseases (IBD) such as Crohn’s disease (CD) and ulcerative colitis are only effective for a minority of patients. Studies have identified a number of IBD-related genes, the products of which may serve as potential targets for new IBD therapies. These studies, however, have primarily focused only on common gene forms, not taking into account variant gene forms which can alter a gene’s function.

In a recent study published in Science Translational Medicine, researchers examined the association between gene variants and Crohn’s disease. To identify the gene variants that significantly impacted Crohn’s Disease risk, the researchers first analyzed the genomes of 50 Crohn’s disease patients with full Ashkenazi Jewish ancestry, a population in which the prevalence of inflammatory bowel diseases is far higher than in non-Jewish Europeans. In total, 4,277 gene variants of interest were identified. The genomes of 1,477 Ashkenazi Jewish patients with Crohn’s disease and 2,614 without were then analyzed for the variants of interest.

The genes found to have the strongest associations with Crohn’s Disease were then analyzed in 589 patients with and 1,019 patients without the disease in North America, Europe, and Israel. Among these genes was LRRK2, the N551K variant of which was found to reduce Crohn’s disease risk and the N2081D variant of which was found to increase it. The K1423K and R1398H variants, which studies have shown to reduce the risk of Parkinson’s disease (PD) when paired with the N551K variant, were found to only slightly increase the risk of Crohn’s disease.

An analysis of Crohn’s disease risk with LRRK2 variants was then conducted on the genomes of 8,314 Ashkenazi Jewish and 16,401 non-Jewish individuals from other studies – 6,538 of which had Crohn’s, 5,570 of which had Parkinson’s disease, and 12,607 healthy participants. The functions and activities of the variants’ gene products were assessed in samples collected from 13 patients. The N2081D variant was associated with earlier development of Crohn’s and the spread of Crohn’s further into the small intestine.  Its gene product, the LRRK2-N2081D protein, had increased activity compared to other variants, similar to the LRRK2-G2019S protein implicated in familial Parkinson’s disease. The N2081D variant also moderately increased and the N551K variant moderately reduced Parkinson’s disease risk, though to lesser degrees than with Crohn’s disease.

The results of this study suggest the N2081D and N551K variants of the LRRK2 gene may be promising targets for future IBD therapies. Moreover, the findings suggest there are shared mechanisms related to LRRK2 underlying both Crohn’s Disease and Parkinson’s disease, understanding which may lead to improvements in the treatment of both conditions.

Written by Raishard Haynes, MBS

Reference: Hul, K.Y. et al. (2018). Functional variants in the LRRK2 gene confer shared effects on risk for Crohn’s disease and Parkinson’s disease. Sci. Transl. Med.10.1126/scitranslmed.aai7795

https://www.medicalnewsbulletin.com/lrrk2-gene-possible-link-crohns-parkinsons-disease/

Trauma and Dementia Patients Given Hope By ‘Flashbulb Memory’ Breakthrough

NEUROSCIENCE NEWS  MARCH 10, 2018
Source: University of Sussex.

Researchers have identified a molecule that appears to play a vital role in long term memory formation.

A snail enjoys a taste of Brighton rock as part of tests into its ability to perform single trial learning.NeuroscienceNews.com image is credited to University of Sussex.

University of Sussex scientists have made a telling breakthrough in detailing the formation of ‘flashbulb memories’, which can help a snail find a sugary treat but also mean a war survivor repeatedly relives their trauma.

The new research brings us much closer to understanding how traumatic memories could be controlled and the cruel blockade on new memories lifted.

Prof George Kemenes and Dr Sergei Korneev at the University of Sussex have identified a specific molecule, a microRNA (miRNA, a very short RNA that does not code any proteins), which plays a key role in ensuring a long-term memory is formed.

The finding could be an important step towards developing treatments for dementia patients as it sheds new light into how two ‘yin and yang’ proteins, CREB1 and CREB2, control the formation or suppression of memories.

The findings from this BBSRC-funded project are significant because it is the first time that specific miRNAs have been shown to play key roles in the forming of long-term memories after a single episode of learning and adds new understanding to how even simple organisms like snails can remember a task after just one attempt.

The discovery, by neuroscientists working in the School of Life Sciences at the University of Sussex and assisted by colleagues at the University of Oxford and in the Koltzov Institute of Developmental Biology of the Russian Academy of Sciences, was established through testing how great pond snails (Lymnaea stagnalis) are able to retain the memory of carrying out a simple task through single trial learning.

In tests, levels of the miRNA Lym-miR-137 were found to significantly increase shortly after single trial learning. This then led to a reduction in the protein Lym-CREB2 mRNA, which is known to play a role in the restriction of memories by acting as a molecular constraint of memory formation.

The results were initially a surprise to the research team as previous experiments on mice showed that reductions in miRNA had enhanced some types of learning and memory.

The team believe that different types of learning are linked with distinct types of miRNA and that a whole complex ‘soup’ of miRNA might be involved in the formation of different types of memory.

The levels of 14 different miRNAs were all found to be altered at differing times during the single-trial learning process.

Prof Kemenes believes that by learning how to control the levels of CREB2 and its counterpart CREB1, a drug could be developed that would relieve the block on forming new memories in dementia patients.

Similarly it has the potential to be used to help repress painful memories within those suffering from post-traumatic stress disorder.

Prof Kemenes said: “Controlling the levels of CREB1 and CREB2 helps animals to retain only the memories that are useful for completing a simple task rather than trying to retain a lot of superfluous information.

“The way snails form memories for this kind of learning is similar to how they are formed within humans.

“The flashbulb formation of a memory that is then retained for a lifetime often involves the creation of a very negative memory such as something particularly traumatic or violent but it can also happen after something much more pleasant like a first kiss.

“The more we can learn about the physical process of forming memories, the more hope there is that we could eventually learn ways to counteract conditions where memories are too traumatic or where new memories are being restricted.”

ABOUT THIS NEUROSCIENCE RESEARCH ARTICLE

Funding: The study was funded by Biotechnology and Biological Sciences Research Council (BBSRC).

Source: Neil Vowles – University of Sussex
Publisher: Organized by NeuroscienceNews.com.
Image Source: NeuroscienceNews.com image is credited to University of Sussex.

Original Research: Open access research in Scientific Reports.

doi:10.1038/s41598-018-22278-w

Abstract

A CREB2-targeting microRNA is required for long-term memory after single-trial learning

Although single-trial induced long-term memories (LTM) have been of major interest in neuroscience, how LTM can form after a single episode of learning remains largely unknown. We hypothesized that the removal of molecular inhibitory constraints by microRNAs (miRNAs) plays an important role in this process. To test this hypothesis, first we constructed small non-coding RNA (sncRNA) cDNA libraries from the CNS of Lymnaea stagnalis subjected to a single conditioning trial. Then, by next generation sequencing of these libraries, we identified a specific pool of miRNAs regulated by training. Of these miRNAs, we focussed on Lym-miR-137 whose seed region shows perfect complementarity to a target sequence in the 3’ UTR of the mRNA for CREB2, a well-known memory repressor. We found that Lym-miR-137 was transiently up-regulated 1 h after single-trial conditioning, preceding a down-regulation of Lym-CREB2 mRNA. Furthermore, we discovered that Lym-miR-137 is co-expressed with Lym-CREB2 mRNA in an identified neuron with an established role in LTM. Finally, using an in vivo loss-of-function approach we demonstrated that Lym-miR-137 is required for single-trial induced LTM.

http://neurosciencenews.com/dementia-flashbulb-memory-trauma-8613/

High Resolution Brain Imaging Provides Clues to Age Related Memory Loss

NEUROSCIENCE NEWS  MARCH 9, 2018
Source: Cell Press.

The decline of signalling in the anterolateral entorhinal cortex has been linked to memory loss associated with aging, a new neuroimaging study reveals.

This figure shows two different brains that are aligned to a common template space for comparison. The yellow in the anterolateral entorhinal cortex of the young brain indicates significant activity, something that is absent in the older brain. NeuroscienceNews.com image is credited to Zachariah Reagh.

As we get older, it’s not uncommon to experience “senior moments,” in which we forget where we parked our car or call our children by the wrong names. But currently there are no good ways to determine which memory lapses are normal parts of aging and which may signal the early stages of a severe disorder like Alzheimer’s disease. In a study appearing March 7 in the journal Neuron, researchers report that data from high-resolution functional brain imaging can be used to show some of the underlying causes for differences in memory proficiency between older and younger adults.

“At the fundamental level, we still understand very little about how aging affects the neural systems that give rise to memory,” says Zachariah Reagh, the study’s first author, who is now a postdoctoral fellow at the University of California, Davis.

The paper reports data from 20 young adults (ages 18 to 31) and 20 cognitively healthy older adults (ages 64 to 89). The participants were asked to perform two kinds of tasks in an fMRI scanner, an object memory task and a location memory task. Because fMRI looks at the dynamics of blood flow in the brain, it enables investigators to determine which parts of their brains the subjects are using in each task.

In the object task, participants learned pictures of everyday objects and were then asked to distinguish them from new pictures. “Some of the pictures were identical to ones they’ve seen before, some were brand new, and others were similar to what they’ve seen before–we may change the color or the size,” says Michael Yassa (@mike_yassa), Director of the Center for the Neurobiology of Learning and Memory at the University of California, Irvine, and the study’s senior author. “We call these tricky items the ‘lures.’ And we found that older adults struggle with these lures. They are much more likely than younger adults to think they’ve seen those lures before.”

The second task was very similar but required subjects to determine during test whether objects changed their location. For this type of memory task, older adults fared quite a bit better. “This suggests that not all memory changes equally with aging,” says Reagh. “Object memory is far more vulnerable than spatial memory, at least in the early stages.” Other studies have shown that problems with spatial memory and navigation do manifest as individuals go down the path to Alzheimer’s disease.

Importantly, by scanning the subjects’ brains while they underwent these tests, the researchers were able to establish a mechanism within the brain for that deficit in object memory.

They found that it was linked to a loss of signaling in the part of the brain called the anterolateral entorhinal cortex. This area was already known to mediate the communication between the hippocampus, where information is first encoded, and the rest of the neocortex, which plays a role in long-term storage. It is also an area that is known to be severely affected in people with Alzheimer’s disease.

“The loss of fMRI signal means there is less blood flow to the region, but we believe the underlying basis for this loss has to do with the fact that the structural integrity of that region of the brain is changing,” Yassa explains. “One of the things we know about Alzheimer’s disease is that this region of the brain is one of the very first to exhibit a key hallmark of the disease, deposition of neurofibrillary tangles.”

In contrast, the researchers did not find age-related differences in another area of the brain connected to memory, the posteromedial entorhinal cortex. They demonstrated that this region plays a role in spatial memory, which was also not significantly impaired in the older subjects. “These findings suggest that the brain aging process is selective,” Yassa adds. “Our findings are not a reflection of general brain aging, but rather specific neural changes that are linked to specific problems in object but not spatial memory.”

To determine whether this type of fMRI scan could eventually be used as a tool for early diagnosis, the researchers plan to expand their work to a sample of 150 older adults who will be followed over time. They will also be conducting PET scans to look for amyloid and tau pathology in their brains as they age.

“We hope this comprehensive imaging and cognitive testing will enable us to figure out whether the deficits we saw in the current study are indicative of what is later to come in some of these individuals,” Yassa says.

“Our results, as well as similar results from other labs, point to a need for carefully designed tasks and paradigms that can reveal different functions in key areas of the brain and different vulnerabilities to the aging process,” Reagh concludes.

ABOUT THIS NEUROSCIENCE RESEARCH ARTICLE

Funding: This study was supported by National Institutes of Health’s National Institute on Aging, a National Science Foundation Graduate Research Fellowship, and fellowships from the UC Irvine Chancellor’s Club and the ARCS and Roche Foundations.

Source: Joseph Caputo – Cell Press
Publisher: Organized by NeuroscienceNews.com.
Image Source: NeuroscienceNews.com image is credited to Zachariah Reagh.
Original Research: Open access research in Neuron.
doi:10.1016/j.neuron.2018.01.039

Abstract

Functional Imbalance of Anterolateral Entorhinal Cortex and Hippocampal Dentate/CA3 Underlies Age-Related Object Pattern Separation Deficits

Highlights

•The anterolateral entorhinal cortex (alEC) is hypoactive in older adults

•The hippocampal dentate and CA3 (DG/CA3) regions are hyperactive in older adults

•Imbalance of DG/CA3-alEC predicts deficits in object mnemonic discrimination

•Imbalance of DG/CA3-alEC is a novel biomarker for age-related memory decline

Summary

The entorhinal cortex (EC) is among the earliest brain areas to deteriorate in Alzheimer’s disease (AD). However, the extent to which functional properties of the EC are altered in the aging brain, even in the absence of clinical symptoms, is not understood. Recent human fMRI studies have identified a functional dissociation within the EC, similar to what is found in rodents. Here, we used high-resolution fMRI to identify a specific hypoactivity in the anterolateral EC (alEC) commensurate with major behavioral deficits on an object pattern separation task in asymptomatic older adults. Only subtle deficits were found in a comparable spatial condition, with no associated differences in posteromedial EC between young and older adults. We additionally linked this condition to dentate/CA3 hyperactivity, and the ratio of activity between the regions was associated with object mnemonic discrimination impairment. These results provide novel evidence of alEC-dentate/CA3 circuit dysfunction in cognitively normal aged humans.

http://neurosciencenews.com/neuroimaging-aging-memory-loss-8606/

Second Parkinson’s Group in Phase 1 Trial Receives ISCO’s Neural Stem Cell Therapy

 MARCH 9, 2018  BY PATRICIA INACIO, PHD

A second group of Parkinson’s patients in a Phase 1 clinical trial have received International Stem Cell Corporation’s neural stem cell therapy.

The main goal of the trial (NCT02452723) at Royal Melbourne Hospital is to see whether ISCO’s stem cell transplants are safe, and patients can tolerate them.

All patients are receiving a specific dose — 30 to 70 million — of the company’s human parthenogenetic neural stem cells (ISC-hpNSC). Researachers are injecting them directly into the striatum and substantia nigra regions of the brain.

Researchers are evaluating safety by measuring the incidence of treatment-related adverse events. An effectiveness measure is how the therapy affects patients’ scores on the Unified Parkinson Disease Rating Scale (UPDRS) after 12 months.

ISCO announced positive interim results from the trial’s first cohort six months after transplant at the Society for Neuroscience’s 47th annual meeting.

Six months after receiving 30 million ISC-hpNSCs, patients in the first trial group showed a 24 percent reduction in their OFF time — a period when levodopa therapy begins to fail and Parkinson’s symptoms return. The therapy extended levodopa’s period of action without dyskinesia — known as ON time — by 19 percent.

All patients improved their mood, with an average increase of 35 % in the Beck Depression Inventory and 33 % in the Parkinson’s Disease Quality of Life Score-39 (PDQ-39). They also improved or retained their cognitive abilities, with an average improvement of 14% in the Cognitive Impairment dimension of the PDQ-39.

They were also able to do better with daily routine activities.

Studies in animal models of the disease showed that ISC-hpNSC was safe and promoted nerve cell regeneration in brain areas treated with the neural stem cells.

“We are pleased to provide an update with the progress of our Parkinson’s disease clinical trial. The completion of the second cohort of patients who received 50 million ISC-hpNSC cells, which represents a biologically active dose in our preclinical studies, is a significant milestone for ISCO. The data from the first cohort of our groundbreaking therapy is already indicating safety and early signals of efficacy,” Russell Kern, ISCO’s executive vice president and chief scientific officer, said in a press release.

https://parkinsonsnewstoday.com/2018/03/09/second-parkinsons-group-in-trial-receives-iscos-neural-stem-cell-therapy/

Parkinson’s disease – myths and facts

March 9, 2018

Parkinson’s disease is an alarming neurodegenerative disorder. This is manifested by progressive deterioration of motor functions due to an inability of neurons to produce dopamine. It is more accurately characterized by slow loss of muscle control, which results in the trembling of the limbs and head while the person is at rest. Stiffness, slowness, and impaired balance are also major hallmarks of this disorder. Mostly this mental abnormality is related to age and occurs in people of near or above 60 years. Surgery is last resort for Parkinson’s disease when medications and other measures fail to improve patient condition. Pallidotomy, Thalamotomy, and deep brain stimulation are three kinds of neurosurgery performed by the best neurosurgeons in Lahore and other mainstream cities of Pakistan through Marham – Find a doctor.

Symptoms:

Primary symptoms of this disorder may include

• Tremor
• Stiffness
• Slowness
• Impaired balance
• Later on a shuffling gait

Some secondary symptoms also associated with it such as

• Anxiety
  • Depression
  •    Dementia
  •    Male erectile dysfunction
  •    Skin problems
  •    Slowed and quieter speech
  •    Urinary frequency

Causes:

This disorder mainly happens due to low levels of dopamine. But which players lower the dopamine level is not unmasked properly. It is hypothesized that some genetic or environmental factors may be responsible for this depletion.

 Genetic factors:

Some genes are notoriously related to onset of this mental disorder such as

• SNCA
• PARK2
• PARK7
• PINK1
• LRKK2

Environmental Factor:

Some environmental factors like some chemicals, inflammation, stress or any other brain abnormality can cause this disorder.

Myths about Parkinson’s disease:

In common community, some misconception related to this mental disorder are present which really needed to correct

• Parkinson’s only affects you physically
• Only older people can be diagnosed with Parkinson’s
• It’s a predictable disease
• Besides taking any prescribed medications, you can’t do anything to help with treatment
• Once you’re diagnosed with Parkinson’s, there’s little to no hope

Facts about Parkinson’s disease:

It mostly shows motor dysfunction related to movement but in reality, some non-motor symptoms are also associated with this disorder like

• Change in speech
• Change in person behavior
• Increased urination
• Cognitive impairments
• In some cases, people less than the age of 40 years also attacked by this mental disorder. It occurs in only 2 percent of all affected person but still, it is a fact.
• Although any lifestyle modifications like healthy diets and regular exercise may help to minimize the symptoms of this deadly disorder.
• With proper management, people with this disorder can live long and enjoy their life in a much better way.

Diagnosis:

Parkinson’s disease can be diagnosed with the help of following parameters

1. At least two major symptoms should be present
2. The onset of symptoms started on one side of the body
3. Symptoms are not appearing due to some secondary causes like medication or strokes in the brain.

Treatment:

Till the date, no proper and exact treatment is present to cure this disease. Some therapies are used to cope this disease in some better way. Like at an early stage of disease levodopa therapy is used. In severe cases, surgery is also done by which surgeon implants electrodes to stimulate brain cells for dopamine production. But some management techniques may help to reduce the severity of symptoms and also onset of the disease such as

• Regular and easy exercise
• Healthy physical activity of limbs
• Healthy diet
• Avoiding the causative agents if any special the person found.

https://dailytimes.com.pk/212594/parkinsons-disease-myths-and-facts/