According to a recent study, people with migraines may have altered connections between the somatosensory cortex and the frontal lobe compared with people who do not experience migraines.
In a study published in the Journal of Headache and Pain, researchers aimed to investigate abnormalities of the frequency-specific somatosensory-related network in patients with migraine by using magnetoencephalography (MEG).
Researchers enrolled 22 patients who experience migraine without aura in the interictal phase and who were right-handed and matched them with 22 health controls by way of sex and age. Investigators sought to examine functional connectivity in the task-related networks of individuals with migraine using MEG.
Right-handed patients with migraine without aura (interictal phase; n = 22; mean age, 29.27; 68.2% women; mean illness duration, 12.70 years; 36% and 64% with bilateral and unilateral migraine, respectively) and sex- and age- matched healthy controls underwent whole head MEG, magnetic resonance imaging, and frequency-specific network analysis. MEG scans were conducted and analyzed in a 1 Hz to 1000 Hz frequency range across multiple bands and a .2 msec electrical stimulus was administered to the right wrist median nerve of each participant.
Scientists at the Marine Biological Laboratory (MBL) have identified gene “partners” in the axolotl salamander that, when activated, allow the neural tube and associated nerve fibers to functionally regenerate after severe spinal cord damage. Interestingly, these genes are also present in humans, though they are activated in a different manner. Their results are published this week in Nature Communications Biology.
“[Axolotls are] the champions of regeneration in that they can regenerate multiple body parts. For example, if you make a lesion in the spinal cord, they can fully regenerate it and gain back both motor and sensory control,” says Karen Echeverri, associate scientist in the Eugene Bell Center for Regenerative Biology and Tissue Engineering. “We wanted to understand what is different at a molecular level that drives them towards this pro-regenerative response instead of forming scar tissue.”
Echeverri’s prior research had shown that, in both axolotls and humans, the c-Fos gene is up-regulated in the glial cells of the nervous system after spinal cord injury. She also knew that c-Fos cannot act alone.
“It’s what we call an obligate heterodimer, so it has to have a partner in life,” says Echeverri. “c-Fos has a different partner in axolotl than it has in humans and this seems to drive a completely different response to injury.”
According to recently published research, vitamins B12 and B9 can lower levels of homocysteine, improve anemia status, and boost physical health in patients with relapsing remitting multiple sclerosis (RRMS).
Current MS research has focused on the role of vitamin 12, folate, and homocysteine. Patients with MS have higher serum homocysteine levels than that of healthy individuals, which is associated with heart disease and can lead to detrimental effects in the nervous system. Lack of vitamin B12 can lead to a disruption in myelination, which is commonly associated with MS.
Researchers enrolled patients with RRMS in a double blinded trial in order to determine how adding vitamin B12 and folic acid would affect serum homocysteine, anemia status, and quality of life.
The study authors enrolled a total of 50 patients with RRMS who had not received vitamin B12 and folate supplements in the past 6 months. All participants completed 2 qualty of life questionnaires, 1 for physical health and the other for mental health, at the start and end of the study. Blood samples and blood pressure readings were collected from every participant, and the group was then split into 2 arms, the vitamin group and the placebo group.
One of the great mysteries of neuroscience may finally have an answer: Scientists at the University of Virginia School of Medicine have identified a potential explanation for the mysterious death of specific brain cells seen in Alzheimer's, Parkinson's and other neurodegenerative diseases.
The new research suggests that the cells may die because of naturally occurring gene variation in brain cells that were, until recently, assumed to be genetically identical. This variation -- called "somatic mosaicism" -- could explain why neurons in the temporal lobe are the first to die in Alzheimer's, for example, and why dopaminergic neurons are the first to die in Parkinson's.
"This has been a big open question in neuroscience, particularly in various neurodegenerative diseases," said neuroscientist Michael McConnell, PhD, of UVA's Center for Brain Immunology and Glia (BIG). "What is this selective vulnerability? What underlies it? And so now, with our work, the hypotheses moving forward are that it could be that different regions of the brain actually have a different garden of these [variations] in young individuals and that sets up different regions for decline later in life."