New discoveries in Parkinson disease, a link between trans fat and dementia, and more
It’s countdown to Thanksgiving, a time to gather round a big hearty meal with your loved ones and count your blessings before hopping for more things to be thankful for next year. But let’s not get ahead of ourselves.
With the holidays imminent, your time is even more valuable than ever. To that end, we’ve curated the latest neuro happenings so you can catch up all in one read, from discoveries of new subtypes of Parkinson disease and links between trans fat and dementia, to more great news about common OTC drugs, we’ve got it covered.
In 1977 Raymond Damadian, MD, completed his work on the first whole-body MRI scanner, which he nicknamed “Indomitable.” Dr. Damadian’s research in cellular sodium and potassium led him to experiment with nuclear magnetic resonance (NMR), which he found could distinguish normal tissues and tumors due to their prolonged relaxation times in T1 and T2—both time constants that determine the rates at which excited protons return to equilibrium, and reach equilibrium or go out of phase with each other, respectively. The rest is history, and in the diagnosis and treatment of neurological disorders and trauma, the use of NMR—renamed MRI because of the negative connotations inherent in the word “nuclear”—has become invaluable.
In the News
Who knew? Parkinson disease (PD) may be a highly varied disease and consist of differing subtypes. In fact, according to a review published in the Journal of Parkinson’s Disease, PD may actually originate in either the brain or in the gut. Researchers reviewed existing evidence that Lewy body disorders, such as PD and dementia with Lewy bodies, are two distinct subtypes—a brain-first subtype and a gut-first subtype—with differing results. The brain-first phenotype enters the brain via the olfactory system and spreads to the brainstem and then the peripheral nervous system (PNS), causing neurologic damage preceded by damage to the peripheral autonomic nervous system (PANS). The gut-first phenotype starts in the PNS of the gut and then spreads to the brain, causing damage to the PANS preceded by neurological damage. Researchers stressed that the possibilities of these differing etiologies of PD must be considered, as should the preventive and treatment strategies their existence brings up.
Constantly in a bad mood? International scientists have just discovered a unique, pea-sized brain receptor in the medial habenula that may regulate negative moods. They published their results in Science. Little is known about the medial habenula, but it is thought to be related to negative emotional states and is the location of this receptor—the glycine gated N-methyl-D-aspartate receptor (NMDA). According to the researchers, the receptor only needs one neurotransmitter to be activated: glycine. This discovery could lead to highly targeted therapies.
You are what you eat. Higher serum levels of trans fat could be a warning sign that dementia will develop later, according to a new study published in Neurology. Trans fatty acids occur naturally in certain meats and dairy foods, and are found mainly in foods that contain partially hydrogenated vegetable oils. Unfortunately, foods that contain less than 0.5 g of trans fat are allowed by the FDA to be labeled as containing 0 g of trans fat. Japanese researchers included 1,628 dementia-free people (average age: 70 years) and divided them into quintiles based on their serum levels of elaidic acid—a biomarker for industrial trans fats. They found that those with higher elaidic acid levels were 50% to 75% more likely to develop Alzheimer disease or dementia later on than those with lower levels. They also discovered that the foods that contributed the most to high levels of trans fat were sweet pastries, margarine, candy, croissants, non-dairy creamers, ice cream, and rice crackers.
Have you seen faces on everyday objects? Pareidolia is Greek for “wrong shape,” and is based on the fine-tuning of human brains to see faces that comprises the entire raison d’être of the fusiform gyrus. It’s something that is evident in us from infancy. This ability is so sophisticated and prevalent in healthy brains, that—in tandem with the brain’s need to find meaning amidst sensory chaos—we find faces in many places where there are no faces at all.
The eyes have it. Good news for MS patients: Paving the way for potential designer therapies for multiple sclerosis (MS), researchers at Johns Hopkins Medicine have identified two complementary genes that may play a role in the vision loss often caused by MS. Using DNA and optical coherence tomography, they report that these genes—C1QA and CR1—may one day serve as markers to monitor and predict the progression of MS. In a study of 835 participants with MS (mean age: 40 years; 74% women), they found that those with genetic changes in the C1QA gene were 71% more likely to have trouble detecting visual contrast, and those with changes in the CR1 gene had a 40% increased risk. These results may be particularly relevant in stopping progressive MS—in which nerve cells begin to die and for which there are currently no therapeutic options—to treat not only disease progression, but nerve cell death. Take that MS!
Normal-but-weird protein in meningiomas. Despite being labeled benign, some grade 1 meningiomas recur earlier and regrow quickly, which are then designated as grade 1.5 tumors. But until now, there was no way of identifying which grade 1 tumors were actually grade 1.5. Talk about an identity crisis. Recently, researchers discovered that certain protein modifications in grade 1 meningiomas could be markers for those that may require more aggressive treatment. Their findings were published in published in Clinical Cancer Research. They used meningioma tissue samples collected from surgical patients over the past 30 years to study protein modifications as a possible clue to do so. After sequencing all proteins produced by the meningiomas, they identified those that were phosphorylated and onto which amino acids of the protein chain the phosphates attached.
In tumors exhibiting grade 1.5 behavior, they noticed a 360% increase in phosphorylation at retinoblastoma 1 (Rb1), a tumor suppressor gene. So, why does this matter? This was surprising because in grade 1.5 meningiomas, the Rb1 gene is not mutated. Despite this, this protein phosphorylation was associated with more aggressive behavior than that exhibited by a true grade 1 tumor. Although researchers don’t know why this protein would phosphorylize, the fact that it does could become a possible marker for tumors that may be grade 1.5 instead of grade 1, and signal the need for closer follow-up and additional treatment.
A long time coming… After 20 years, researchers may have finally discovered an effective way to test for prion diseases, which are fatal neurodegenerative conditions caused by the accumulation of misfolded copies of a naturally occurring protein. They recently published their results in PLoS ONE. To date, this is the only published diagnostic method for quick, noninvasive prion detection in living subjects—a monumental achievement and a milestone in biomedical technology. Let’s give these folks the round of applause they deserve. The team developed peptoid beads that can detect the misfolded proteins that cause prion diseases, as well as Alzheimer disease and Parkinson diseases—the hallmarks of which are also large, aggregated proteins. Peptoids are artificial compounds that mimic peptides. The new peptoid beads consist of tiny magnets covered in peptoids that mimic part of the prion protein. Added to a liquid, the peptoid beads will attach to misfolded prion protein aggregates—like Velcro, according to the researchers—while ignoring normal proteins. The misfolded proteins are then run through the misfolded protein assay developed by Novartis. The peptoid beads can detect asymptomatic disease carriers, and possibly be optimized to screen blood and blood products, according to the researchers.
A wonder drug? Aspirin may protect against aneurysm growth and future rupture in patients with intracranial aneurysms, according to a recent review published in the Journal of Neurosurgery. Researchers included 146 patients with a total of 375 intracranial aneurysms who had undergone surgical or endovascular treatment for one aneurysm that had ruptured or was at risk for rupture. Of the 146 aneurysm that were treated, the remaining 229 were ≤ 5 mm in diameter and monitored for growth for at least 5 years. They found an association between the use of aspirin and a decreased rate of aneurysm growth. These are promising results, especially in light of the fact that aneurysm growth increases the risk for ruptures, as well as the lack of any treatment to arrest aneurysm growth and subsequent progression to rupture. At this point we’re wondering: What can’t aspirin do?
Treating ‘puff of smoke’ disease. Looks like we’ve got a lot to be thankful for this year. In children with moyamoya disease, indirect bypass surgery may effect long-term improvement in overall clinical outcomes, as well as prevent recurrent stroke, according to a longitudinal and cross-sectional analysis published in Stroke. This is particularly good news because this progressive disease is incurable, and will not improve without treatment. Researchers followed 629 children with moyamoya disease who had undergone indirect bypass surgery at a single center for more than 5 years. They found that overall clinical outcomes were favorable in 95% of patients, and the annual risk of symptomatic infarction in the operated hemisphere was 0.08% and risk of hemorrhage was 0.04%. Impressively, 10-year event-free survival rates for symptomatic infarction were 99.2%, and for hemorrhage, 99.8%. ‘Tis the season to celebrate.
A tale of rats and rapamycin. Rapamycin may prevent age-related brain vascular deterioration by preserving the integrity of brain circulation and memory, according to a preclinical study published in Aging Cell. Rats that were fed low-dose rapamycin during “rat middle age” (19 months) and continued through “advanced rat age” (34 months) maintained consistently similar blood circulation to the brain, compared with untreated rats that demonstrated typical age-related vascular changes. This makes sense in that the target of rapamycin (TOR) controls both cell growth and aging. These results bolster the idea that TOR also drives the loss of synapses and cerebral blood flow related to aging. Further research is ongoing, and if successful, may point to a role for rapamycin in preventing Alzheimer dementia someday. Still, these rats got nothing on Benjamin Button.
New in Patient Management
More to love? Children who are obese may also have reduced cortical thickness, which may lead to weaker executive functioning, according to a recent study published in Cerebral Cortex. Researchers analyzed data from 2,700 children aged 9-11 years, and found a correlation between higher BMI and reduced global cortical thickness, bilateral prefrontal region thickness, and executive functioning. Reductions in executive function were partially caused by reduced thickness in the rostral medial and superior fontal cortex, the inferior frontal gyrus, and the lateral orbitofrontal cortex. They postulated that prefrontal cortical changes caused by childhood obesity could cause altered regulation of inhibitory control and risk-taking behavior, as well as difficulties in future weight control.
You’re never too old to hit the gym. It’s not news that exercise is beneficial for the brain. But researchers are constantly finding new benefits to getting your exercise on. One recent study found improvements in cardiorespiratory fitness brought on by exercise are strongly associated with a lower risk of dementia, no matter how late in life you start exercising. Studies linking physical fitness and reduced risk of dementia are numerous and consistent, but this study was different because researchers measured fitness levels in more than 30,000 subjects twice, 10 years apart. This way, they were able to assess how changes in fitness over time are related to dementia risk.
Researchers published the results of the HUNT2 study in The Lancet Public Health, and concluded that not just being physically unfit, but that remaining unfit over time was an independent risk factor for dementia and dementia-related mortality. Plus, they discovered that it’s never too late to start exercising. The reduction in dementia risk was even more apparent in those who were 60 years old at baseline. An increase in cardiorespiratory fitness of 1 met was associated with a 16% reduction in the risk of dementia and a 10% reduced risk of dementia-related mortality. And because no treatment is currently available for dementia prevention, this is big news—that something as simple as increased fitness over time can lower one’s dementia risk. That’s one health recommendation you won’t want to ‘forget’.
Skip the supplements? Don’t hold your breath if you’re taking vitamin D or omega-3 supplements to reduce systemic inflammation, which has been long tied to the development of neurodegenerative diseases, such as Alzheimer disease. Researchers from Brigham & Women’s Hospital recently published these findings in Clinical Chemistry. To reach this conclusion, they analyzed data from the VITamin D and OmegA-3 trial (VITAL), and tested levels of three known biomarkers of inflammation—interleukin-6 (IL-6), tumor necrosis factor-receptor 2, and high sensitivity C-reactive protein (hsCRP)—at baseline and after patients took vitamin D (2,000 IU/d), omega-3s (1 g/d) or both for 1 year. None of the regimens decreased any of these levels after 1 year, and in those taking vitamin D, IL-6 levels actually rose by 8.2%. The only good news they had to report was that among those with lower intakes of fish at baseline, omega-3 supplementation decreased hsCRP levels.
Bad day? Try not to stress about it. In a secondary analysis of the PRoFESS trial, the largest trial to date of patients with potential recurrent stroke, researchers assessed the association between increased blood pressure variability and recurrent ischemic stroke. Each year, nearly 185,000 ischemic strokes occur in patients who suffered a previous stroke. Recurrent stroke carries significantly higher morbidity and mortality, and hypertension is the most prevalent modifiable risk factor. These researchers found that for every 10-point increase in blood pressure variability, there was an HR of 1.15 for recurrent ischemic stroke, 1.19 for major cardiovascular events, and 1.24 for all-cause mortality. They found no significant association between blood pressure variability and hemorrhagic stroke.
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Upcoming Medical Meetings
9th World Congress of Neuroendoscopy, in Orlando, FL, November 21-24, 2019
2019 Advances in the Management of Epilepsy, in New Orleans, LA, December 6, 2019
31st Annual Pan Philadelphia Neurosurgery Conference, in Philadelphia, PA, December 6, 2019
American Epilepsy Society (AES) 2019 Annual Meeting, Baltimore, MD, December 6-10, 2019