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 have Parkinson's diseases as well and thought it would be nice to have a place where updated news is in one place. That is why I began this blog.
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Summary: Researchers report the brain connections that are key to cognition and complex thinking skills are most effected as we age.
Source: University of Edinburgh.
This image shows how ageing affects the health of most white matter pathways with age, but some more strongly than others. NeuroscienceNews image is adapted from the University of Edinburgh press release.
Impact of ageing on brain connections mapped in major scan study.
Brain connections that play a key role in complex thinking skills show the poorest health with advancing age, new research suggests.
Connections supporting functions such as movement and hearing are relatively well preserved in later life, the findings show.
Scientists carrying out the most comprehensive study to date on ageing and the brain’s connections charted subtle ways in which the brain’s connections weaken with age.
Knowing how and where connections between brain cells – so-called white matter – decline as we age is important in understanding why some people’s brains and thinking skills age better than others.
Worsening brain connections as we age contribute to a decline in thinking skills, such as reasoning, memory and speed of thinking.
Researchers from the University of Edinburgh analysed brain scans from more than 3,500 people aged between 45 and 75 taking part in the UK Biobank study.
Researchers say the data will provide more valuable insights into healthy brain and mental ageing, as well as making contributions to understanding a range of diseases and conditions.
The study was published in Nature Communications journal.
Dr Simon Cox, of the University of Edinburgh’s Centre for Cognitive Ageing and Cognitive Epidemiology (CCACE), who led the study, said: “By precisely mapping which connections of the brain are most sensitive to age, and comparing different ways of measuring them, we hope to provide a reference point for future brain research in health and disease.
“This is only one of the first of many exciting brain imaging results still to come from this important national health resource.”
Professor Ian Deary, Director of CCACE, said: “Until recently, studies of brain scans with this number of people were not possible. Day by day the UK Biobank sample grows, and this will make it possible to look carefully at the environmental and genetic factors that are associated with more or less healthy brains in older age.”
Professor Paul Matthews of Imperial College London, Chair of the UK Biobank Expert Working Group, who was not involved in the study, said: “This report provides an early example of the impact that early opening of the growing UK Biobank Imaging Enhancement database for access by researchers world-wide will have.
“The large numbers of subjects in the database has enabled the group to rapidly characterise the ways in which the brain changes with age – and to do so with the confidence that large numbers of observations allow.
“This study highlights the feasibility of defining what is typical, to inform the development of quantitative MRI measures for decision making in the clinic.”
ABOUT THIS NEUROSCIENCE RESEARCH ARTICLE
Funding: The University of Edinburgh Centre for Cognitive Ageing and Cognitive Epidemiology receives funding from the Medical Research Council (MRC) and the Biotechnology and Biological Sciences Research Council (BBSRC).
UK Biobank was established by the Wellcome Trust, MRC, Department of Health, Scottish Government and the Northwest Regional Development Agency. It has had funding from the Welsh Assembly Government, British Heart Foundation and Diabetes UK. UK Biobank is hosted by the University of Manchester and supported by the NHS.
Image Source: NeuroscienceNews.com image is adapted from the University of Edinburgh press release.
Original Research:Full open access research for “Ageing and brain white matter structure in 3,513 UK Biobank participants” by Simon R. Cox, Stuart J. Ritchie, Elliot M. Tucker-Drob, David C. Liewald, Saskia P. Hagenaars, Gail Davies, Joanna M. Wardlaw, Catharine R. Gale, Mark E. Bastin & Ian J. Deary in Nature Communications. Published online December 15 2016 doi:10.1038/NCOMMS13629
Ageing and brain white matter structure in 3,513 UK Biobank participants
Quantifying the microstructural properties of the human brain’s connections is necessary for understanding normal ageing and disease. Here we examine brain white matter magnetic resonance imaging (MRI) data in 3,513 generally healthy people aged 44.64–77.12 years from the UK Biobank. Using conventional water diffusion measures and newer, rarely studied indices from neurite orientation dispersion and density imaging, we document large age associations with white matter microstructure. Mean diffusivity is the most age-sensitive measure, with negative age associations strongest in the thalamic radiation and association fibres. White matter microstructure across brain tracts becomes increasingly correlated in older age. This may reflect an age-related aggregation of systemic detrimental effects. We report several other novel results, including age associations with hemisphere and sex, and comparative volumetric MRI analyses. Results from this unusually large, single-scanner sample provide one of the most extensive characterizations of age associations with major white matter tracts in the human brain.
“Ageing and brain white matter structure in 3,513 UK Biobank participants” by Simon R. Cox, Stuart J. Ritchie, Elliot M. Tucker-Drob, David C. Liewald, Saskia P. Hagenaars, Gail Davies, Joanna M. Wardlaw, Catharine R. Gale, Mark E. Bastin & Ian J. Deary in Nature Communications. Published online December 15 2016 doi:10.1038/NCOMMS13629
Earlier this week, the Foundation signed on to a letter to President-elect Trump and congressional leadership explaining the critical role that high quality and affordable health insurance plays in helping our community access essential treatments and care. We expressed our desire to work together in creating a health care system that benefits all Americans.
Over 70 patient groups joined the letter. The full text can be found below:
December 14, 2016
President-elect Donald J. Trump
1800 F Street, NW
Washington, DC 20405
Dear President-elect Trump:
The next four years present an opportunity to build a health policy agenda for all Americans. We write on behalf of the millions of Americans living with chronic, serious and life-threatening diseases who need access to affordable health insurance and quality health care.
The individuals we represent have daily health care demands that can span the course of a lifetime. Every day, this population grapples with managing their health needs while navigating complex insurance plans within a fragmented delivery system.
Americans who rely heavily on the health care system must be assured of adequate and affordable insurance that covers their health care needs. The high cost of care and inadequate insurance has led many to skip or delay care. They deserve a health care system that will help enable them to lead longer, healthier lives.
Policies that expand access to coverage, such as those that prevent preexisting condition exclusions and allow young people to remain on their parents’ plans until age 26, are critically important to this population. These policies alone, however, are not enough to ensure meaningful access to health care.
We look forward to working with you and your Administration to ensure that the needs of the patients we represent are fully considered as the health insurance and health care systems are reevaluated.
American Brain Coalition
American Lung Association
American Parkinson Disease Association
American Partnership for Eosinophilic Disorders
Amyloidosis Support Groups Inc.
Association of Gastrointestinal Motility Disorders, Inc.
Batten Disease Support and Research Association
Friedreich's Ataxia Research Alliance
GBS|CIDP Foundation International
Global Genes - Allies in Rare Disease
Hannah's Hope Fund for Giant Axonal Neuropathy
Hepatitis Foundation International
Hide & Seek Foundation for Lysosomal Disease Research
Hope for Hypothalamic Hamartomas
Huntington’s Disease Society of America
Immune Deficiency Foundation
International Bipolar Foundation
International Foundation for Functional Gastrointestinal Disorders
The International Essential Tremor Foundation
Interstitial Cystitis Association
Kids v Cancer
The Marfan Foundation
The Michael J. Fox Foundation
Moebius Syndrome Foundation
Multiple Myeloma Research Foundation
Muscular Dystrophy Association
Myotonic Dystrophy Foundation
National Alliance of State & Territorial AIDS Directors
Bladder Cancer Advocacy Network (BCAN)
CADASIL: Together We Have Hope
Child Neurology Foundation
Citizens United for Research in Epilepsy
Cutaneous Lymphoma Foundation
Cystic Fibrosis Foundation
Dystonia Medical Research Foundation
Familial Hypercholesterolemia Foundation
The Fibrous Dysplasia Foundation
FORCE: Facing Our Risk of Cancer Empowered
Foundation for Prader-Willi Research
National Alliance on Mental Illness
National Alopecia Areata Foundation
National Multiple Sclerosis Society
National Organization for Rare Disorders
National PKU Alliance
National Tay-Sachs & Allied Diseases Association
NephCure Kidney International
Neurodegeneration with Brain Iron Accumulation Disorders Association
Summary: Researchers have developed a new technique that is able to rejuvenate organs in animals and extend their life span.
Source: Salk Institute.
Salk Institute researchers discover that partial cellular reprogramming reversed cellular signs of aging such as accumulation of DNA damage. (Left) Progeria mouse fibroblast cells; (right) progeria mouse fibroblast cells rejuvenated by partial reprogramming. NeuroscienceNews image is credited to Salk Institute.
New technique rejuvenated organs and helped animals live longer.
Graying hair, crow’s feet, an injury that’s taking longer to heal than when we were 20—faced with the unmistakable signs of aging, most of us have had a least one fantasy of turning back time. Now, scientists at the Salk Institute have found that intermittent expression of genes normally associated with an embryonic state can reverse the hallmarks of old age.
This approach, which not only prompted human skin cells in a dish to look and behave young again, also resulted in the rejuvenation of mice with a premature aging disease, countering signs of aging and increasing the animals’ lifespan by 30 percent. The early-stage work provides insight both into the cellular drivers of aging and possible therapeutic approaches for improving human health and longevity.
“Our study shows that aging may not have to proceed in one single direction,” says Juan Carlos Izpisua Belmonte, a professor in Salk’s Gene Expression Laboratory and senior author of the paper appearing in the December 15, 2016, issue of Cell. “It has plasticity and, with careful modulation, aging might be reversed.”
As people in modern societies live longer, their risk of developing age-related diseases goes up. In fact, data shows that the biggest risk factor for heart disease, cancer and neurodegenerative disorders is simply age. One clue to halting or reversing aging lies in the study of cellular reprogramming, a process in which the expression of four genes known as the Yamanaka factors allows scientists to convert any cell into induced pluripotent stem cells (iPSCs). Like embryonic stem calls, iPSCs are capable of dividing indefinitely and becoming any cell type present in our body.
“What we and other stem-cell labs have observed is that when you induce cellular reprogramming, cells look younger,” says Alejandro Ocampo, a research associate and first author of the paper. “The next question was whether we could induce this rejuvenation process in a live animal.”
While cellular rejuvenation certainly sounds desirable, a process that works for laboratory cells is not necessarily a good idea for an entire organism. For one thing, although rapid cell division is critical in growing embryos, in adults such growth is one of the hallmarks of cancer. For another, having large numbers of cells revert back to embryonic status in an adult could result in organ failure, ultimately leading to death. For these reasons, the Salk team wondered whether they could avoid cancer and improve aging characteristics by inducing the Yamanaka factors for a short period of time.
To find out, the team turned to a rare genetic disease called progeria. Both mice and humans with progeria show many signs of aging including DNA damage, organ dysfunction and dramatically shortened lifespan. Moreover, the chemical marks on DNA responsible for the regulation of genes and protection of our genome, known as epigenetic marks, are prematurely dysregulated in progeria mice and humans. Importantly, epigenetic marks are modified during cellular reprogramming.
Using skin cells from mice with progeria, the team induced the Yamanaka factors for a short duration. When they examined the cells using standard laboratory methods, the cells showed reversal of multiple aging hallmarks without losing their skin-cell identity.
“In other studies scientists have completely reprogrammed cells all the way back to a stem-cell-like state,” says co-first author Pradeep Reddy, also a Salk research associate. “But we show, for the first time, that by expressing these factors for a short duration you can maintain the cell’s identity while reversing age-associated hallmarks.”
Encouraged by this result, the team used the same short reprogramming method during cyclic periods in live mice with progeria. The results were striking: Compared to untreated mice, the reprogrammed mice looked younger; their cardiovascular and other organ function improved and—most surprising of all—they lived 30 percent longer, yet did not develop cancer. On a cellular level, the animals showed the recovery of molecular aging hallmarks that are affected not only in progeria, but also in normal aging.
“This work shows that epigenetic changes are at least partially driving aging,” says co-first author Paloma Martinez-Redondo, another Salk research associate. “It gives us exciting insights into which pathways could be targeted to delay cellular aging.”
Lastly, the Salk scientists turned their efforts to normal, aged mice. In these animals, the cyclic induction of the Yamanaka factors led to improvement in the regeneration capacity of pancreas and muscle. In this case, injured pancreas and muscle healed faster in aged mice that were reprogrammed, indicating a clear improvement in the quality of life by cellular reprogramming.
“Obviously, mice are not humans and we know it will be much more complex to rejuvenate a person,” says Izpisua Belmonte. “But this study shows that aging is a very dynamic and plastic process, and therefore will be more amenable to therapeutic interventions than what we previously thought.”
The Salk researchers believe that induction of epigenetic changes via chemicals or small molecules may be the most promising approach to achieve rejuvenation in humans. However, they caution that, due to the complexity of aging, these therapies may take up to 10 years to reach clinical trials.
ABOUT THIS PSYCHOLOGY RESEARCH ARTICLE
Other authors included: Aida Platero-Luengo, Fumiyuki Hatanaka, Tomoaki Hishida, Mo Li, David Lam, Masakazu Kurita, Ergin Beyret, Toshikazu Araoka, Eric Vazquez-Ferrer, David Donoso, Jose Luis Roman, Jinna Xu and Concepcion Rodriguez of the Salk Institute; Estrella Nuñez Delicado of Universidad Católica San Antonio de Murcia; Gabriel Núñez of the University of Michigan Medical School; Josep Maria Campistol of Hosplital Clinic of Barcelona and Isabel Guillén and Pedro Guillén of Fundación Dr. Pedro Guillén.
Funding: The work and the researchers involved were supported in part by a National Institutes of Health Ruth L. Kirschstein National Research Service Award Individual Postdoctoral Fellowship, the Muscular Dystrophy Association, Fundación Alfonso Martin Escudero, the Hewitt Foundation, the Uehara Memorial Foundation, the Nomis Foundation, a JSPS Postdoctoral Fellowship for Research Abroad, the University of California, San Diego, the G. Harold and Leila Y. Mathers Charitable Foundation, The Leona M. and Harry B. Helmsley Charitable Trust (2012-PG-MED002), The Glenn Foundation, Universidad Católica San Antonio de Murcia (UCAM) and Fundación Dr. Pedro Guillén.
Image Source: NeuroscienceNews.com image is credited to Salk Institute.
Video Source: The video is credited to Salk Institute.
Original Research:Full open access research for “In Vivo Amelioration of Age-Associated Hallmarks by Partial Reprogramming” by Alejandro Ocampo, Pradeep Reddy, Paloma Martinez-Redondo, Aida Platero-Luengo, Fumiyuki Hatanaka, Tomoaki Hishida, Mo Li, David Lam, Masakazu Kurita, Ergin Beyret, Toshikazu Araoka, Eric Vazquez-Ferrer, David Donoso, Jose Luis Roman, Jinna Xu, Concepcion Rodriguez Esteban, Gabriel Nuñez, Estrella Nuñez Delicado, Josep M. Campistol, Isabel Guillen, Pedro Guillen, and Juan Carlos Izpisua Belmonte in Cell. Published online December 15 2016 doi:10.1016/j.cell.2016.11.052
In Vivo Amelioration of Age-Associated Hallmarks by Partial Reprogramming
•Partial reprogramming erases cellular markers of aging in mouse and human cells
•Induction of OSKM in progeria mice ameliorates signs of aging and extends lifespan
•In vivo reprogramming improves regeneration in 12-month-old wild-type mice
Aging is the major risk factor for many human diseases. In vitro studies have demonstrated that cellular reprogramming to pluripotency reverses cellular age, but alteration of the aging process through reprogramming has not been directly demonstrated in vivo. Here, we report that partial reprogramming by short-term cyclic expression of Oct4, Sox2, Klf4, and c-Myc (OSKM) ameliorates cellular and physiological hallmarks of aging and prolongs lifespan in a mouse model of premature aging. Similarly, expression of OSKM in vivo improves recovery from metabolic disease and muscle injury in older wild-type mice. The amelioration of age-associated phenotypes by epigenetic remodeling during cellular reprogramming highlights the role of epigenetic dysregulation as a driver of mammalian aging. Establishing in vivo platforms to modulate age-associated epigenetic marks may provide further insights into the biology of aging.
“In Vivo Amelioration of Age-Associated Hallmarks by Partial Reprogramming” by Alejandro Ocampo, Pradeep Reddy, Paloma Martinez-Redondo, Aida Platero-Luengo, Fumiyuki Hatanaka, Tomoaki Hishida, Mo Li, David Lam, Masakazu Kurita, Ergin Beyret, Toshikazu Araoka, Eric Vazquez-Ferrer, David Donoso, Jose Luis Roman, Jinna Xu, Concepcion Rodriguez Esteban, Gabriel Nuñez, Estrella Nuñez Delicado, Josep M. Campistol, Isabel Guillen, Pedro Guillen, and Juan Carlos Izpisua Belmonte in Cell. Published online December 15 2016 doi:10.1016/j.cell.2016.11.052
Summary: While marijuana can initially help with symptoms of anxiety and depression, it can be detrimental to mental health when used long term, a new study reports.
Source: Colorado State University.
Researchers found that those respondents categorized with subclinical depression, who reported using the drug to treat their depressive symptoms, scored lower on their anxiety symptoms than on their depressive symptoms - so, they were actually more depressed than they were anxious. The same was true for self-reported anxiety sufferers: they were found to be more anxious than they were depressed. NeuroscienceNews.com image is for illustrative purposes only.
For those suffering depression or anxiety, using cannabis for relief may not be the long-term answer.
That’s according to new research from a team at Colorado State University seeking scientific clarity on how cannabis – particularly chronic, heavy use – affects neurological activity, including the processing of emotions.
Researchers led by Lucy Troup, assistant professor in the Department of Psychology, have published a study in PeerJ describing their findings from an in-depth, questionnaire-based analysis of 178 college-aged, legal users of cannabis. Recreational cannabis became legal in Colorado in 2014. Since then, seven other states have enacted legalization for recreational use, while many others allow medical use.
“One thing we wanted to focus on was the significance of Colorado, the first state to legalize recreational cannabis, and its own unique population and use that occurs here,” Troup said.
Through the study, which was based solely upon self-reported use of the drug, the researchers sought to draw correlations between depressive or anxious symptoms and cannabis consumption.
They found that those respondents categorized with subclinical depression, who reported using the drug to treat their depressive symptoms, scored lower on their anxiety symptoms than on their depressive symptoms - so, they were actually more depressed than they were anxious. The same was true for self-reported anxiety sufferers: they were found to be more anxious than they were depressed.
In other words, “if they were using cannabis for self-medication, it wasn’t doing what they thought it was doing,” explained co-author Jacob Braunwalder, a recently graduated student researcher in Troup’s lab.
Study co-author Jeremy Andrzejewski led the development of the questionnaire, called R-CUE (Recreational Cannabis Use Evaluation), that took a deep dive into users’ habits, including questions about whether users smoked the drug, or consumed stronger products like hash oils or edibles. The researchers are particularly motivated to study biochemical and neurological reactions from higher-tetrahydracannabinol (THC) products available in the legal market, which can be up to 80-90 percent THC.
The researchers are quick to point out that their analysis does not say that cannabis causes depression or anxiety, nor that it cures it. But it underscores the need for further study around how the brain is affected by the drug, in light of legalization, and by some accounts, more widespread use in Colorado since legalization.
For example, said Andrzejewski, “there is a common perception that cannabis relieves anxiety.” Yet research has yet to support this claim fully, he said.
Graduate student and co-author Robert Torrence pointed to past research that shows that chronic use reduces naturally occurring endocannabinoids in the brain, which are known to play a role physiological processes including mood and memory.
“There is research to suggest that cannabis can help with anxiety and depression in the beginning, but it has the reverse effect later on,” said Torrence, a U.S. Army veteran who is especially interested in studying cannabis’ effectiveness in treating post-traumatic stress disorders.
Due to the federal government’s stringent regulations around researching cannabis, which is a schedule I drug, the general public’s perception of how it affects the brain is often based in “mythos,” Braunwalder said. “We want to add more information to the entire body of research.”
There are currently no CSU research labs that administer cannabis to study participants, as administration of the drug for research would require special licensing and security.
Moving forward, the researchers want to refine their results and concentrate on respondents’ level and length of exposure to legally available high-THC products like concentrates and hash oils, around which there has been little scientific inquiry.
“It is important not to demonize cannabis, but also not to glorify it,” Troup said. “What we want to do is study it, and understand what it does. That’s what drives us.”
Image Source: NeuroscienceNews.com image is in the public domain.
Original Research:Full open access research for “The relationship between cannabis use and measures of anxiety and depression in a sample of college campus cannabis users and non-users post state legalization in Colorado” by Lucy J. Troup, Jeremy A. Andrzejewski, Jacob T. Braunwalder, and Robert D. Torrence in PeerJ. Published online December 8 2016 doi:10.7717/peerj.2782
The relationship between cannabis use and measures of anxiety and depression in a sample of college campus cannabis users and non-users post state legalization in Colorado
As part of an ongoing research program into the relationship between cannabis use and emotion processing, participants were assessed on their level of cannabis exposure using the Recreational Cannabis Use Examination, a measure developed specifically to assess cannabis use in Colorado post state legalization. Three groups were created based on self-reported use: a control group who have never used, a casual user group and a chronic user group. Each participant also completed two measures of mood assessment, the Center for Epidemiologic Studies Depression Scale and the State-Trait Anxiety Inventory. Relationships between cannabis use groups and scores on these measures were then analyzed using both correlations and multivariate analysis of variance. Results indicate a relationship between casual cannabis use and scoring highly for depressive symptomatology on the Center for Epidemiologic Studies Depression Scale. There were no significant relationships between cannabis use and scores on the State-Trait Anxiety Inventory.
“The relationship between cannabis use and measures of anxiety and depression in a sample of college campus cannabis users and non-users post state legalization in Colorado” by Lucy J. Troup, Jeremy A. Andrzejewski, Jacob T. Braunwalder, and Robert D. Torrence in PeerJ. Published online December 8 2016 doi:10.7717/peerj.2782
As regular, long-time readers of this column already know, I’ve had Parkinson’s Disease for more than seven years now. Actually it’s probably more like nine years because I had the symptoms for about two years before finally accepting the diagnosis. This column is simply to update readers on how I’m doing because hardly a day goes by that I don’t get a polite inquiry.
Loretta had been telling me, since sometime in 2008, that she thought I might have Parkinson’s because we knew a couple of people who “suffered” from the disease and she thought I exhibited some the same peculiar physical symptoms as our acquaintances. She had also read a couple of magazine articles on the subject and then found some information on the internet to support her theory.
I fought my wife’s diagnosis for well over a year because, in my opinion, my symptoms did not resemble those of the folks who had positive diagnosis and I rarely believe anything that comes off the internet. If you want to prove that earth is square you can, if you search hard enough, find a website to support that theory.
My biggest problem, initially, was a lack of balance. I simply had problems walking or even standing erect without something to lean on. I wore the tips off a couple of walking canes and my hands shook so badly I had trouble signing my name.
My primary care doctor finally talked me into seeing a neurologist. Dr. Bellanger suspected that I might have Parkinson’s but he also knew that I was in deep denial. I later found out that it is fairly common for people with Parkinson’s to go to great lengths to prove that they have something else. I was already being treated for diabetes, for example, and spent many hours trying to link my symptoms to that disease even though metformin had my sugar levels under pretty good control.
Anyway, the neurologist told me he wasn’t sure what I had but he didn’t think it was Parkinson’s. That was exactly what I wanted to hear. He also told me there was a surefire way to find out and that was to try a medication called senimet. He also said that if I had noticeable improvements in mobility and the tremors lessened, it meant the medicine was working and that it only worked on Parkinson’s Disease by replacing certain chemicals the brain could no longer produce. He said it might take 30 days to start working and scheduled another appointment six weeks down the road.
So I wobbled out of his office on my walker and literally smirked at Loretta. That was in early December of 2010. On Christmas Day, I was still trembling so badly that I couldn’t open presents without assistance and I still needed a cane or the walker to get around.
But by New Year’s Day, I no longer needed a walking device and I discovered that I could write a column in about two hours, a feat that had previously taken the better part of two days because I couldn’t hold my hands still enough to type before the medicine started working.
Since that time, I’ve had two strokes that have had the residual effect of making my left hand useless for typing and now I only use the thumb and middle finger of my right hand for that effort but I’m back up to about 45 words per minute on a typing test. And that’s probably a good thing because it makes me think before I write something. Unfortunately, it does not make me think before I speak and Loretta frequently tells me I could use some help in that regard.
I am one of the very lucky ones when it comes to Parkinson’s. I believe I have mentioned here before that the doctors tell me I could be a poster boy for the medication. I’ve had better results than more than 95 percent of patients using senimet to treat the disease.
I’ve also run out a couple of times for a couple of days and discovered, the hard way, just how dependent I am on what has proven to me to be a life-changing miracle drug. I try to keep a minimum of a 30-day supply on hand at all times.
As I’ve said several times before, there’s no “suffering” associated with my personal experience with Mr. Parkinson but there is a lot of aggravation and annoyance and I suspect that just about everybody has their fair share of those.
Having Parkinson's disease (PD) itself affects cognition, but new research shows that adding orthostatic hypotension (OH) has an even greater impact on cognitive function in patients with PD.
A new study shows patients with PD and those with PD plus OH had similar mild cognitive impairment compared with matched controls while in the supine position, but there was a significant adverse effect on cognition only in the PDOH group when patients were in the upright position.
"Patients with Parkinson's disease need to be screened for orthostatic hypotension regardless of whether or not they are reporting symptoms," said lead author, clinical neuropsychologist Justin Centi, PhD, Department of Psychological and Brain Sciences, Boston University, Massachusetts (now working for a private practice in Boston).
"The presence of orthostatic hypotension on clinical examination should alter the approach to management to include consideration for postural effects on cognition."
When possible, added Dr Centi, clinicians should consider referrals for neuropsychological testing with a battery that includes repeat assessment in a variety of postures.
And, because the cognitive deficits that emerged in the study included problems with visuospatial processing, clinicians should consider nonmotor factors as possibly contributing to problems, such as gait instability and falls, he said.
The study included 55 patients without dementia. Among them were 18 normotensive PD patients with OH and a group of 19 normotensive PD patients without OH, matched for disease duration, motor symptom severity, and levodopa equivalent dosages. The study also included 18 controls matched for age, sex, and education.
None of the study participants met criteria for dementia. There were no baseline differences in blood pressure or heart rate.
OH was defined as a sustained reduction in systolic blood pressure of at least 20 mm Hg or a reduction in diastolic blood pressure of at least 10 mm Hg during the first 3 minutes of standing or while on a tilt table.
Many of the patients with OH were asymptomatic, and none reported severe symptoms of OH.
Researchers tested patients on neuropsychological performance while supine, then upright (60 degrees from flat), and then supine again. They looked at attention/executive function, memory, and visuospatial skills, which are domains that are typically problematic for patients with PD.
Compared with controls, both PD groups showed impaired cognition while supine and were impaired on several executive measures and had poorer memory encoding while tilted upright.
This pattern, said the authors, is seen in as many as 55% of patients with PD and is most likely the result of functional disconnection.
Following the tilt, PD patients with OH showed a greater posture-mediated impairment than controls on several tests, including Arithmetic, Symbol Search, Phonemic Fluency, the Stroop test (color-word condition), memory encoding (P < .01), and Visual Dependence (P = .01).
Compared with patients with PD without OH, PD patients with OH showed a significantly greater effect of postural change on Symbol Search (P < .01), CERAD (Consortium to Establish a Registry for Alzheimer's Disease) total score (P < .01), and Visual Dependence (P < .01).
"The pattern of deficits was reflective of an exacerbation of already vulnerable domains, including information processing speed, working memory, learning, verbal fluency, and visuospatial processing," noted Dr Centi.
The cognitive declines were reversed when patients were returned to the supine position.
Because this transient change was not seen in patients with PD —without OH or in controls, the results imply "a direct effect of OH," the authors conclude.
Worsening cognition as a result of OH has a significant impact on daily living — for example, it makes shopping, counting change, and tracking conversations a challenge, they note.
The findings are important because they suggest that neuropsychological testing in PD, and perhaps all conditions where OH is frequently concomitant, has failed to effectively capture the full nature of cognitive deficits, Dr Centi said.
"This has major implications for both clinical and research-related endeavors. Moreover, studies that rely on functional neuroimaging — for example, fMRI [functional MRI] and PET [positron emission tomography] — which is conducted only in the supine position, may need to consider a more limited scope when interpreting their findings."
Dr Centi stressed that because none of the study patients rated symptoms as moderate or severe when tilted, reliance on their self-report would likely fail to identify many cases of OH in the clinical setting.
Dr Centi and his colleagues recommend that, at a minimum, all patients with PD be screened regardless of whether or not they report common symptoms, for example, lightheadedness.
And as some patients may have delayed-onset OH, clinicians should consider a more comprehensive autonomic evaluation if they don't have the time or resources to fully assess for this presentation in the office setting, said Dr Centi.
In an accompanying editorial, Laura S. Boylan, MD, Department of Neurology, New York University School of Medicine, New York, and Lambros Messinis, PhD, Neuropsychology Section Department of Neurology, University of Patras Medical School, Greece, agreed that If the study findings are found to be generalizable, "the implications are potentially far-reaching."
An improved understanding of underlying mechanisms between systemic blood pressure and cognitive function is needed and should span subspecialty disciplines of clinical and basic research, but this would be "a challenge in an age of silos," Dr Boylan and Dr Messinis note.
They noted that limitations of the study included its sample size, use of repeated measures, and use of cognitive tests of unknown ecologic validity/applicability to daily life.
While all patients were normotensive at baseline, some were receiving blood pressure medication, which may be confounding, they said. They also pointed out that tilt-table positioning is not equivalent to standing up.
The study was "interesting" and the research methods and statistical analysis "appear appropriate and reasonable," said Christopher Hess, MD, assistant professor, neurology, and co-director, Movement Disorders Fellowship, University of Florida Center for Movement Disorders and Neurorestoration, Gainesville, when asked to comment for Medscape Medical News.
"This is an important study which suggests that focusing on the treatment of orthostatic hypotension might improve cognition in patients with PD," said Dr Hess.
"The findings reinforce the need to do sitting and standing blood pressure measurements in patients with PD as not all patients in the study described the symptoms of orthostatic hypotension."
Further studies with larger sample sizes would help to determine whether the results of the study are more generalizable to routine cognitive screening and neuropsychiatric testing, added Dr Hess.
The study was funded by a National Research Service Awards training grant (National Institutes of Health, National Institute of Neurological Disorders and Stroke) as part of Dr Centi's doctoral dissertation. Dr Centi, Dr Boylan, and Dr Messinis have disclosed no relevant financial relationships.
New research finds a link between the nutrient lutein and "crystallized intelligence," the ability to use the skills and knowledge acquired during one’s life.
The older I get, the more I nod knowingly with an audible “mmm hmm” when I hear the adage, “Youth is wasted on the young.” On the flipside, of course, is that maturity brings with it all of the wisdom picked up along the way. Now if only we could just remember everything we learned and put it to use. Therein lies the rub.
But now research brings to light a way in which “crystallized intelligence” – the ability to use learned knowledge and experience – might be preserved in older adults. The discovery? That the plant pigment lutein may be playing a role.
We get lutein primarily by eating leafy green vegetables (kale tops the USDA list for lutein content), cruciferous vegetables such as broccoli, or egg yolks (thanks to the diet of chickens). It's also worth noting that many studies have previously shown that lutein and its partner zeaxanthin reduce the risk of chronic eye diseases, including age-related macular degeneration (AMD) and cataracts.
According to study leader Marta Zamroziewicz from the University of Illinois and professor Aron Barbey, lutein accumulates in the brain, embedding in cell membranes, where it likely plays "a neuroprotective role.”
"Previous studies have found that a person's lutein status is linked to cognitive performance across the lifespan," Zamroziewicz says. "Research also shows that lutein accumulates in the gray matter of brain regions known to underlie the preservation of cognitive function in healthy brain aging."
Participants in the new study included 122 healthy adults between the ages of 65 to 75 who solved problems and answered questions on a standard test of crystallized intelligence. Researchers then looked at blood samples for blood serum levels of lutein and analyzed the participants' brains using MRI to measure the volume of different brain structures.
The researchers found that participants with higher blood serum levels of lutein tended to do better on tests of crystallized intelligence. Serum lutein levels reflect only recent dietary intakes, notes the study's press release, but are associated with brain concentrations of lutein in older adults, which reflect long-term dietary intake. Those with higher serum lutein levels also tended to have thicker gray matter in the parahippocampal cortex, a brain region that, like crystallized intelligence, is preserved in healthy aging.
"Our analyses revealed that gray-matter volume of the parahippocampal cortex on the right side of the brain accounts for the relationship between lutein and crystallized intelligence," Barbey says. "This offers the first clue as to which brain regions specifically play a role in the preservation of crystallized intelligence, and how factors such as diet may contribute to that relationship."
So the moral of the story could be: Youth is wasted on the young, but it doesn’t have to be wasted on the old? Or in other words … eat your vegetables.