I Ask This Of You!

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.

I am not responsible for it's contents. I am just a copier of information searched on the computer. Please understand the copies are just that, copies and at times, I am unable to enlarge the wording or keep it uniformed as I wish.

This is for you to read and to always keep an open mind.

Please discuss this with your doctor, should you have any questions, or concerns.

Never do anything without talking to your doctor. I do not make any money from this website. I volunteer my time to help all of us to be informed. I will not accept any information about Herbal treatments curing Parkinson's, dementia and etc. It will go into Spam.

This is a free site for all with no advertisements.

Thank you for visiting!

Thursday, September 20, 2018

Dementia: New risk factor examined

September 20, 2018  By Tim Newman

Over the years, scientists have identified a number of risk factors for dementia. However, according to the most recent study, that list might be incomplete.

Understanding the risk factors for dementia is more important than ever.

Dementia describes a group of symptoms that include a decline in memory and cognitive abilities.
There are a number of conditions labeled as dementias, the most common of which is Alzheimer's disease.
Certain risk factors for these conditions are now understood. The most well-known is age; they become more likely as we get older.
Other factors include a sedentary lifestyle, smoking, excessive alcohol consumption, hypertension, high cholesterol levels, being overweight, a lack of social contact, and head injuries.
Because dementia is prevalent — affecting an estimated 44 million people, globally — and there is still no cure, understanding the full range of risk factors is important.
As the population grows collectively older, the importance of understanding and minimizing the risk of dementia grows ever more vital. If risk factors can be minimized, onset can be pushed back; as the authors of the new study write, "small delays in its onset and progression could significantly reduce its estimated future burden."
A group of researchers recently published a paper in the BMJ that might add another risk factor to this list: air pollution.

Air pollution and dementia

Air pollution has previously been linked to respiratory diseases and cardiovascular conditions, such as stroke. However, to date, links with dementia have remained unclear.
While previous studies have hinted at a relationship between air pollution exposure and dementia, many have not been high quality. To remedy this, a group of researchers set out to reach a more definitive answer.
To do this, the researchers estimated levels of noise and air pollution across Greater London in the United Kingdom. Next, they took data from the Clinical Practice Research Datalink, a nonprofit research service that has been collecting data since 1987.
In all, the team used the medical records of almost 131,000 people who were aged 50–79 in 2004, none of whom had been diagnosed with dementia.
From the participants' addresses, the scientists could estimate their individual exposure to a range of pollutants, including traffic noise. These estimates were backed up by recorded measurements on site.
The pollutants of interest were nitrogen dioxide (NO2), fine particulate matter (PM2.5), and ozone (O3).

'A 40 percent greater risk'

Using these health records, the team tracked the health of each participant, following them until a diagnosis of dementia, deregistration from the doctor's office, or death, whichever came first. On average, this follow-up lasted 7 years. Of the whole group, 2,181 people (1.7 percent) developed dementia.
The analysis showed that people whose exposure to NO2 was in the top fifth had a 40 percent greater risk of being diagnosed with dementia than those in bottom fifth. When they analyzed PM2.5 levels, there was a similar relationship.
Even after controlling for relevant factors — such as smoking and diabetes — the results remained significant. Levels of O3 and noise pollution did not increase dementia risk.
However, as the authors are quick to note, this is an observational study; it is not possible to draw firm conclusions about causation. Other as yet unknown factors might be driving the relationship. There is also the possibility that the findings are only relevant for the city of London.
It is also important to note that diseases such as Alzheimer's can take many years to develop and be diagnosed, so longer studies are preferable.
If the link between air pollution and dementia is real, what might be driving it? There is a range of potential ways in which air pollution could impact the brain, one of which the authors outline:
Traffic-related air pollution has been linked to poorer cognitive development in young children, and continued significant exposuremay produce neuroinflammation and altered brain innate immune responses in early adulthood.  
Because air pollution already causes substantial health problems, lowering levels would be of great benefit to the public; it might also bring down dementia risk. Even if the reduction in risk is minimal, because dementia is so prevalent, it could make a huge difference


20th September 2018 

Sarcopenia is the loss of muscle mass, strength and function related to ageing. Sarcopenia and frailty are found in up to one-third of the general elderly population. Both are associated with major adverse health outcomes such as nursing home placement, disability, decreased quality of life. For more information go to :

In people who have Parkinson's Disease who were in care the prevalence of sarcopenia was found to be much higher, as it was 55% and only 8% in people who did not have Parkinson's Disease. Frailty was detected in 35% of people with Parkinson's Disease.

In those people with Parkinson's Disease who were not in care, 33% had sarcopenia and 22% had frailty. Both sarcopenia and frailty were significantly associated with longer disease duration of Parkinson's Disease, higher motor impairment, higher Hoehn and Yahr stages, decreased quality of life, higher frequency of falls, a higher non-motor symptom burden, institutionalization, and higher care levels.

Regular exercise, or dietary changes and an increase in the intake of high protein foods, or the use of certain drugs can reverse sarcopenia or help to prevent sarcopenia from occurring. For more information go to :

Reference : Gerontology [2018] Sep 10 [Epub ahead of print] (M.Peball, P.Mahlknecht, M. Werkmann, K.Marini, F.Murr, H.Herzmann, H.Stockner, Marzi, B.Heim, A. Djamshidian, P.Willeit, J.Willeit, S.Kiechl, D.Valent, F.Krismer, G.K.Wenning, M.Nocker, K.Mair, W.Poewe, K.Seppi)

Complete abstract :

Genomic dark matter activity connects Parkinson's and psychiatric diseases

September 20, 2018, Brigham and Women's Hospital

Illustration depicting transcribed noncoding elements (TNE or enhancer RNAs) in the brain Credit: Clemens Scherzer, Brigham and Women's Hospital

Dopamine neurons are located in the midbrain, but their tendril-like axons can branch far into the higher cortical areas, influencing how we move and how we feel. New genetic evidence has revealed that these specialized cells may also have far-reaching effects, implicating them in conditions that range from Parkinson's disease to schizophrenia. 

Using a new technique known as laser-capture RNA seq, that involves cutting out dopamine neurons from a human brain section with a laser, investigators from Brigham and Women's Hospital and Harvard Medical School have cataloged more than 70,000 novel elements active in these brain cells. Their results are published this week in Nature Neuroscience.

"We found that a whopping 64 percent of the human genome—the vast majority of which is 'dark matter' DNA that does not code proteins—is expressed in  in the human ," said Clemens Scherzer, MD, a neurologist and genomicist who directs the APDA Center for Advanced Parkinson's Disease Research and leads the Precision Neurology Program at BWH. "These are critical and specialized cells in the human brain, which are working sluggishly in Parkinson's disease, but might be overactive in schizophrenia."

Scherzer's team developed laser-capture RNAseq to precisely dissect out dopamine neurons from the brain and perform ultradeep RNA sequencing on cells. From 86 post-mortem brains, the team was able to extract more than 40,000 dopamine neurons. While other groups have focused on protein-producing messenger RNA, Scherzer and colleagues wanted to catalog the cells' entire RNA content, which required taking a much deeper dive.

In total, they found 71,022 transcribed noncoding elements (so called TNEs). Many of these TNEs (pronounced "teenies") are active enhancers—sites that act as regulatory "switches" for turning on specialized functions for billions of neurons in the brain. Many of the TNEs the team unearthed are novel and had never before been described in the brain. Working with collaborators in England, Scherzer and colleagues tested several of the TNEs in preclinical models, including zebrafish, finding evidence that many were active in brain development.

Scherzer and first-author Xianjun Dong, Ph.D., who are also Principal Investigators at the Ann Romney Center at BWH, originally set out to study dopamine neurons to gain insights into Parkinson's but found that many of the genetic variants associated with schizophrenia, addiction and other neuropsychiatric diseases were also enriched in these elements.

"This work suggests that noncoding RNAs active in dopamine neurons are a surprising link between genetic risk, Parkinson's and psychiatric disease," said Scherzer. "Based on this connection we hypothesize that the risk variants might fiddle with the gene switches of dopamine-producing ."

The team has also made an encyclopedia of RNA content for publicly available so that other investigators can look up any protein-coding or noncoding target for biomarkers and therapeutics for Parkinson's and psychiatric diseases through the webportal

More information: Xianjun Dong et al, Enhancers active in dopamine neurons are a primary link between genetic variation and neuropsychiatric disease, Nature Neuroscience (2018).  DOI: 10.1038/s41593-018-0223-0

Journal reference: Nature Neuroscience

Analysis of sea squirt embryo reveals key molecules in dopaminergic neuron differentiation

September 20, 2018, University of Tsukuba

Researchers at the University of Tsukuba have revealed two molecules in the brain of a sea squirt that specify the development of a hypothalamus-like region, also shedding light on how different parts of the brain form in more complex organisms.

The human  is exceedingly complex, consisting of various regions with particular functions and approximately 100 billion . This complexity has presented a major challenge in understanding this organ and how it develops, particularly in view of the ethical issues associated with research on humans.

In a new study reported in Genes and Development, a research team centered at University of Tsukuba has developed a novel approach for revealing how the brain forms via the creation of different types of  using a sea squirt, a simple organism that is a precursor to the vertebrates. Using this approach, the team identified two molecules that are vital for the development of a region of this species' brain analogous to the hypothalamus in humans, which has potential implications across the field of neuroscience.

The sea squirt is a useful model for studying  as it presents some basic features of all vertebrates at an early evolutionary stage, while having a central nervous system containing only 177 neurons. The researchers took advantage of this simplicity by performing the sequencing of RNA for single cells across whole embryos, revealing that two molecules, Ptf1a and Meis, are vital for the emergence of dopaminergic neurons/coronet cells, a simple early form of the hypothalamus.

"We were able to sequence the RNA from about 5000 cells from sea squirt embryos and identified the particular neurons that we wished to focus on by finding dopaminergic marker genes in their expression profiles," corresponding author Yasunori Sasakura says. "One gene, Ptf1a, was only expressed in dopaminergic neurons/coronet cells, but not in any other neurons, so we then analyzed it further."

The team showed that blocking this gene's expression led to a failure of these specific neurons to form, while aberrantly expressing this gene throughout the nervous system converted most of the neurons into this specific type.

"We then classified the cells expressing Ptf1a into different subgroups and found that those that most completely differentiated into dopaminergic neurons also expressed the gene Meis," Takeo Horie says. "Our analyses showed that these two transcription factors work in tandem to stimulate production of these neurons, which also has important implications for how the hypothalamus forms in humans."

The team couldn't have made a discovery of this kind without the novel approach of single-cell RNA sequencing and manipulations such as gene knockout and overexpression. This characterization of the way in which different subpopulations of neurons are created, albeit in a simple precursor to the human hypothalamus, could help in the fight against human diseases involving  deficiencies such as Parkinson's disease.

More information: Takeo Horie et al. Regulatory cocktail for dopaminergic neurons in a protovertebrate identified by whole-embryo single-cell transcriptomics, Genes & Development (2018). DOI: 10.1101/gad.317669.118

Journal reference: Genes & Development

Provided by: University of Tsukuba

Wednesday, September 19, 2018

Excellent Choices for Parkinson’s Disease Care


While searching for a movement disorders doctor, I happened upon a government listing for Parkinson’s Disease (PD) Centers of Excellence, which fascinated me.
According to the Parkinson’s Foundation, PD Centers of Excellence deliver care worldwide to more than 127,000 patients. The centers “advance research to improve the lives of everyone with Parkinson’s treated at centers and beyond, and for future generations.” They also “provide patient education programs, community outreach programs and specialized Parkinson’s training for healthcare professionals.” The movement disorders team at each hospital must fulfill a list of criteria, which in turn leads to these specific centers being recognized by their medical peers as “leaders in PD care.”
The Parkinson’s Foundation says that folks from all the centers come together at least once a year to bring the latest information or offer updates on care initiatives and research. Each center is required to be recertified every three years, in a process that includes looking at the accomplishments of each center.
I was amazed. The patients who can see a movement disorder specialist in one of these centers must be so well taken care of. I think one of the main reasons is that there are accountability and integrity within these organizations. What does that mean to us as patients? We are better cared for, and the care we receive should be, according to their mission, top quality.
I happened upon a Center of Excellence because one of my doctors was a part of one. I can vouch for the fact that they truly exemplify “excellence.”
If you are not satisfied with the care you are receiving, feel your medical team may not be up to date with the latest care for you as their patient, or you just want to see if a change in care is warranted, get in touch with one near you (see the listings below). It’s definitely worth the call and maybe even the drive.

Centers of Excellence in the United States


– Barrow Neurological Institute, Muhammad Ali Parkinson Center


– University of Southern California, Parkinson’s Disease and Other Movement Disorders Center
– University of California, San Francisco, Parkinson’s Disease Clinic and Research Center (415) 476-9276
– The Parkinson’s Institute and Clinical Center, Sunnyvale, (408) 542-5646

District of Columbia

– Georgetown University Hospital, (202) 444-2333


– University of Florida, Parkinson’s Disease and Movement Disorders Center, Department of Neurology, (352) 273-5550
– University of Miami, Miller School of Medicine, Parkinson’s Disease and Movement Disorders Center
– University of South Florida, Parkinson’s Disease and Movement Disorders Center, (813) 844-4547


– Health Sciences University, Department of Neurology, (706) 721-2798


– Northwestern University, Parkinson’s Disease and Movement Disorders Center, Chicago, (312) 503-4397
– Rush University Medical Center, Chicago


– University of Kansas Medical Center, Parkinson’s Disease and Movement Disorder Center, (913) 588-7179


– University of Louisville, Movement Disorder Program, (502) 852-3655


– Johns Hopkins Medical Institute, Parkinson’s Disease and Movement Disorders Center, (410) 955-8795


– Massachusetts General Hospital, Wang Ambulatory Care Center, (617) 724-9234
– Beth Israel Deaconess Medical Center, Parkinson’s Disease and Movement Disorders Center, (617) 667-2699


– Struthers Parkinson’s Center, (952)993-5214

New York

– SUNY Downstate Medical Center/Kings County Hospital, Parkinson’s Disease and Related Disorders Clinic, (718) 270-7371
– Beth Israel Medical Center, The Movement Disorders Center, Phillips Ambulatory Care Center, (212) 844-6134
– Columbia University Medical Center, New York
– Mount Sinai School of Medicine, Bendheim Parkinson and Movement Disorder, (212) 241-2477
– NYU Langone Medical Center, Parkinson’s Disease and Movement Disorders Center, (646) 505-5744
– University of Rochester Medical Center, Movement and Inherited Neurological Disorders Unit, (585) 276-3987

North Carolina

– University of North Carolina at Chapel Hill, School of Medicine, Department of Neurology, (919) 966-5549
– Duke University Medical Center, Department of Neurology, (919) 684-5128


– Oregon Health and Science University, Parkinson Center of Oregon, (503) 494-5620


– University of Pennsylvania, Parkinson’s Disease and Movement Disorders Center, (215) 829-7273


– Vanderbilt University Medical Center, Vanderbilt Parkinson’s Disease Center, (615) 936-5517


– Baylor College of Medicine, Parkinson’s Disease Center and Movement Disorders Clinic, (713) 798-3951


– Booth Gardner Parkinson’s Care Center, (425) 899-3123
Note: Parkinson’s News Today is strictly a news and information website about the disease. It does not provide medical advice, diagnosis or treatment. This content is not intended to be a substitute for professional medical advice, diagnosis, or treatment. Always seek the advice of your physician or another qualified health provider with any questions you may have regarding a medical condition. Never disregard professional medical advice or delay in seeking it because of something you have read on this website. The opinions expressed in this column are not those of Parkinson’s News Today or its parent company, BioNews Services, and are intended to spark discussion about issues pertaining to Parkinson’s disease.

Study to Explore Art Therapy for Improving Visuospatial, Motor Function in Parkinson’s Patients


A new exploratory study intends to assess the benefit of art therapy in improving visuospatial function and gait in Parkinson’s disease patients.
The ExplorArtPD study (NCT03178786) is currently recruiting participants in New York City. More information on enrollment can be found here.
Due to the variety of Parkinson’s motor and non-motor symptoms, including visuospatial dysfunction — loss of space orientation, motion perception, and target localization — effective treatments require multidisciplinary approaches involving physical therapy, occupational therapy, psychological support, family counseling, and palliative care.
When these approaches fail, complementary therapeutic strategies, such as art therapy, may hold potential to help patients restore functional independence and maintain their quality of life.
Although the source of visusospatial dysfunction in Parkinson’s is not fully understood, altered visual function has been consistently shown, with subsequent impaired ability to drive, read, and write, and increased anxiety and depression, as well as a greater risk of falls.
Given the lack of specific therapeutic strategies for visuospatial dysfunction associated with Parkinson’s disease, researchers at the Marlene and Paolo Fresco Institute for Parkinson’s and Movement Disorders at NYU Langone Health developed an art therapy intervention protocol that includes psychotherapy and art creation to address visuospatial dysfunction and psychological needs of Parkinson’s patients.
The study is aimed at determining the characteristics of visuospatial exploration and its neural basis as assessed by clinical and behavioral tests, neuropsychological inventories, eye tracking, gait analysis, and brain magnetic resonance imaging (MRI). Researchers also intend to assess the therapeutic impact of art therapy on visuospatial dysfunction and gait in Parkinson’s patients.
“According to our preliminary data [art therapy] appears to be a safe, non-invasive, reproducible modality of intervention that could be administered to [Parkinson’s] patients with potential ease of recruitment,” the authors wrote.
The study has an anticipated enrollment of 40 participants, 20 of whom will have a clinical diagnosis of Parkinson’s disease and a Hoehn and Yahr scale stage of 2-3 — stage 2 meaning symptoms on both sides of the body, but no balance impairment, and stage 3 referring to balance impairment and mild to moderate disease. They must also have no history of clinically active eye abnormalities, and be eligible to undergo brain MRI scans. Researchers will also include 20 age-matched participants without Parkinson’s disease who will serve as controls.
Parkinson’s patients will undergo open-label art therapy and assessments both before the completion of art projects (baseline) and after completion (follow-up), while control participants will only undergo baseline assessments. In patients with motor fluctuations, the assessments will be made in the “on” state, when motor disability is milder and assessments can be performed with a lower risk of physical or psychological fatigue.
Art therapy will consist of 20 consecutive sessions lasting 90 minutes each, approximately twice per week for a maximum of 14 weeks. It will be administered by credentialed professionals with a master’s degree in art therapy. The approach will favor group dynamics, mutual support, and encouragement through shared projects. A total of nine different projects are planned, which will be introduced every two sessions.
Art materials — pastels, clay, ornamental fabrics, watercolor, paint and brushes — and projects will be tailored to personality traits, artistic preferences, level of artistic engagement, and physical limitations. Each project will focus on different aspects of visuospatial function, such as the ability to comprehend, manipulate, and create 3D artifacts using multisensory integration and hand-eye coordination, and organizing artifacts in 2D, which implies abstraction skills and sequential planning.
Eye tracking, taking place over 70-90 minutes, will be assessed with a head-mounted, infrared-based device during the performance of neuropsychological inventories, namely the Rey-Osterrieth Complex Figure Test and a modified, multiple-choice version of the Benton Visual Retention Test, on different aspects of visuospatial and executive skills. Connectivity between different brain areas will be determined with MRI scans lasting 45-90 minutes.
Emotional well-being, daily quality of life, and motor and non-motor symptoms of Parkinson’s will be assessed using different scales, questionnaires, and tests, along with three computerized tasks to assess visual discrimination, perception and visual-executive functions.
Art assessment will use the House-Tree-Person Projective Technique, which involves drawing three familiar themes — a house, a tree, and a person — to collect information about the person’s intentions and associations at both conscious and unconscious levels. It provides insight into an individual’s cognitive, psychological, emotional, and physical state when drawing.
Art therapy will begin approximately six weeks after the baseline phase of the study. Medical monitoring will carefully assess adverse events, although the team expects risks to be minimal.
“We believe that both patients and the scientific community will benefit from the knowledge gained from this study,” the researchers wrote. “A favorable outcome in this pilot study would support the development of further trials aiming to validate the therapeutic potential of this novel paradigm of neurorehabilitation.”

Parkinson's Pilot Study Reveals Dance Therapy May Benefit Patients


Using dance as a therapeutic strategy may benefit patients with Parkinson’s disease by improving their motor function, results of a pilot study suggest.
Parkinson’s disease is mainly recognized by its progressive motor symptoms including tremor, muscle rigidity, and impaired gait and balance. Several non-motor symptoms are also experienced by patients, including cognitive impairment, fatigue, mood disorders, and sleep disturbances, all of which can be disabling and lead to a significant decrease in quality of life.
Anti-parkinsonian therapies focus on easing and managing the motor symptoms of the disease, but their use can be limited by the presence of non-motor issues. In addition, effective treatments for non-motor symptoms are not always available.
Given the complex symptom-treatment landscape of the disease, there is increased interest from both patients and caregivers in pursuing mind-body interventions, such as dance therapy, which have the potential to simultaneously address both the motor and non-motor symptoms of the disease.

Dance requires the practice of fluid movements and postures while maintaining full body control, which can address many of the motor symptoms associated with Parkinson’s. In addition, dance can improve patients’ emotional, cognitive, and social well-being as a result of listening to music and interacting with other people, potentially reducing the common non-motor symptoms of Parkinson’s.
Dance therapy differs from traditional dance classes because it not only focuses on the aesthetic and recreational features of the activity, but also includes the biopsychological status of the subject.
According to the American Dance Therapy Association, “dance/movement therapy is the psychotherapeutic use of movement to promote emotional, social, cognitive and physical integration of the individual.”
A team led by researchers at Northwestern University in Illinois evaluated the benefits of dance therapy in nine Parkinson’s patients, and compared it with the effects of support group therapy in four patients, who served as the control group.
Patients enrolled in the dance group had a mean age of 66.4 and mean Movement Disorder Society Unified Parkinson’s Disease Rating Scale (MDS-UPDRS) motor score of 27.6 points. The control group was older, with a mean age of 75.5, and had worse motor scores, a mean of 40.8 points. The UPDRS is a comprehensive 50-question assessment of both motor and non-motor symptoms associated with Parkinson’s.
Dance therapy sessions lasted 60 minutes and were conducted once a week, over 10 weeks. The exercises were tailored on an individual basis to incorporate different levels of functional capacity. The sessions focused on an understanding of how movement influences mood and mental health; enhanced balance, gait, and coordination; and expression of thoughts, feelings, and emotions through movement and dance.
The certified dance therapist who conducted the dance therapy sessions also led the support group, “which involved education about how movement influences mood and mental health, ways to incorporate movement and dance into daily life, and exploration of feelings and emotions in a supportive group environment,” according to the researchers.
Seven of the nine patients in the dance group and all participants in the control group completed the study, attending at least 70 percent of the classes. Only one participant in the dance therapy group developed mild low back pain, but it was unclear whether this was due to the dance intervention.
After completing the 10-week intervention, participants were questioned about their satisfaction with the program.
In general, patients in the dance group enjoyed the therapy sessions, with seven patients reporting benefits from them, while the other two felt neutral. Six patients in the dance group and two in the support group noted they would attend similar classes in the future and would recommend the program to other Parkinson’s patients. Only one patient in the control group did not enjoy or benefit from the classes, conveying disappointment at not having been included in the dance therapy group.
An evaluation of symptoms after the completion of the study revealed a 2.37-point reduction in motor disability scores on the MDS-UPDRS III in the dance therapy group compared with the control group. Patients who received dance therapy also improved their ability to perform daily living activities, with a 0.36-point difference in MDS-UPDRS II scores relative to the control group. Some positive changes in non-motor symptoms such as fatigue and cognition were also reported, but these were not significant.
“Dance may be effective in targeting motor symptoms of Parkinson’s disease because it incorporates the stretching and strengthening of muscles, and increases flexibility throughout the body, which may help maintain balance in people with Parkinson’s,” the researchers wrote.
“Another possibility is that practice of dance may activate areas of the brain that normally show reduced activation in Parkinson’s,” they added.
Because this study only included a small number of patients, researchers were not able to fully determine the complete impact of these interventions in disease manifestations.
Additional studies in a larger patient population over longer periods of time are necessary to further explore the potential of dance therapy, in particular its ability to improve motor function in Parkinson’s patients.
“This is the first study of dance therapy as a psychotherapeutic movement intervention in Parkinson’s disease,” the authors noted. In general, its results support “the feasibility of a dance therapy intervention [in this population],” the said.

Zombie cells found in brains of mice prior to cognitive loss

September 19, 2018, Mayo Clinic

Zombie cells are the ones that can't die but are equally unable to perform the functions of a normal cell. These zombie, or senescent, cells are implicated in a number of age-related diseases. And with a new letter in Nature, Mayo Clinic researchers have expanded that list.

In a mouse model of  disease, scientists report that senescent  accumulate in certain brain cells prior to cognitive loss. By preventing the accumulation of these cells, they were able to diminish  aggregation, neuronal death and memory loss.

"Senescent cells are known to accumulate with advancing natural age and at sites related to diseases of aging, including osteoarthritis; atherosclerosis; and neurodegenerative diseases, such as Alzheimer's and Parkinson's," says Darren Baker, Ph.D., a Mayo Clinic molecular biologist and senior author of the paper. 

"In prior studies, we have found that elimination of senescent cells from naturally aged mice extends their healthy life span."

In the current study, the team used a model that imitates aspects of Alzheimer's disease.

"We used a  that produces sticky, cobweb like tangles of tau protein in neurons and has genetic modifications to allow for senescent cell elimination," explains first author Tyler Bussian, a Mayo Clinic Graduate School of Biomedical Sciences student who is part of Dr. Baker's lab. "When senescent cells were removed, we found that the diseased animals retained the ability to form memories, eliminated signs of inflammation, did not develop neurofibrillary tangles, and had maintained normal brain mass." They also report that pharmacological intervention to remove senescent cells modulated the clumping of tau proteins.

Also, the team was able to identify the specific type of cell that became senescent, says Dr. Baker.

"Two different brain cell types called 'microglia' and 'astrocytes' were found to be senescent when we looked at brain tissue under the microscope," says Bussian. "These cells are important supporters of neuronal health and signaling, so it makes sense that senescence in either would negatively impact neuron health."

The finding was somewhat surprising, explains Dr. Baker, because at the time their research started, a causal link between  cells and neurodegenerative disease had not been established.

"We had no idea whether  actively contributed to disease pathology in the brain, and to find that it's the astrocytes and microglia that are prone to senescence is somewhat of a surprise, as well," says Dr. Baker.

In terms of future work, Dr. Baker explains that this research lays out the best-case scenario, where prevention of damage to the brain avoided the disease state. "Clearly, this same approach cannot be applied clinically, so we are starting to treat animals after disease establishment and working on new models to examine the specific molecular alterations that occur in the affected cells," says Dr. Baker.

More information: Clearance of senescent glial cells prevents tau-dependent pathology and cognitive decline, NatureDOI: 10.1038/s41586-018-0543-y,

Journal reference: Nature

Provided by: Mayo Clinic