10 Important Neuroscience Developments in 2013
Updated October 12, 2014.
Written or reviewed by a board-certified physician. See About.com's Medical Review Board.
Every year the Editorial Advisory Board selects some of that year’s best scientific publications in the field of neuroscience. A “best-of” list is clearly a matter of some personal opinion, and cannot be considered complete, so I don't feel too bad about altering that list somewhat with some other selections of advances in neuroscience that made the news in 2013. Due to the ever-changing nature of science, is entirely possible that some of the selections will turn out to be not very important after all, while an overlooked publication will turn out to have huge implications in the future.
Caveats aside, here’s some of 2013’s neuroscientific highlights, in no particular order.
Sleep and the Brain’s Garbage Disposal
Why sleep is so important that we spend a third or so of our lives unconscious has been a major medical mystery. In 2012 the laboratory of Maiken Nedergaard described (and named) a glymphatic system that relies on cerebrospinal fluid to flush toxins such as beta-amyloid out of the brain. In 2013, the researchers discovered that the levels of toxins changed most while sleep. If this is accurate, we need to sleep so that our brains can take out the garbage.
Source:
Xie L, Kang H, Xu Q, Chen MJ, Liao Y, et al. Sleep Drives Metabolite Clearance from the Adult Brain. Science 18 October 2013: Vol. 342 no. 6156 pp. 373-377
Lab-Grown Mini-Brains…
Okay, really this is a model, but still, scientists used stem cells to create small and primitive versions of our own brains, with different cell types and firing neurons. While very far off from a full scale working human brain, this allows a new way to study diseases, especially of brain development.
Source:
Madeline A. Lancaster, Magdalena Renner, Carol-Anne Martin, et al. Cerebral organoids model human brain development and microcephaly. Nature, doi:10.1038/nature12517, epub Aug. 28
Move It or Lose It?
Need motivation to do more exercise? We’ve suspected for some time that physical exercise was one of the best ways to keep your brain sharp, but in 2013 researchers discovered one of the reasons why. A previously identified protein in muscles is increased in endurance exercise in the hippocampus of mice, and increases levels brain-derived neurotrophic factor (BDNF). BDNF is a substance that is also associated with better functioning of the hippocampus, responsible for learning and short-term memory.
Source:
Wrann CD, White JP, Salogiannis J, Laznik-Bogoslavski D, Wu J, et al. Exercise Induces Hippocampal BDNF through a PGC-1a/FNDC5 Pathway Cell Metabolism, Volume 18, Issue 5, 649-659, 10 October 2013
No Benefit to IA tPA Over tPA Alone in Acute Stroke
This paper demonstrated that additional treatment with endovascular treatments with intra-arterial tissue plasminogen activator tPA for ischemic stroke after tPA was administered intravenously did not have any benefit over giving tPA alone. What this means for other endovascular procedures for acute stroke, such as those using stent retrievers remain to be worked out.
Source:
Broderick JP, Palesch YY, Demchuk AM et al. Interventional Management of Stroke (IMS) III Investigators: Endovascular therapy after intravenous t-PA versus t-PA alone for stroke. N Engl J Med. 2013; 368(13): 1265.
An Insight into ALS and FTD
C9ORF72 has been tied with amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD). The gene consists of hundreds to thousands of GGGGCC repeats. These papers described how dipeptide proteins accumulate into inclusions as a result, providing some explanation for how the gene mutation causes these diseases.
Sources:
Ash PE, Bieniek KF, Gendron TF, et al. Unconventional translation of C9ORF72 GGGGCC expansion generates insoluble polypeptides specific to c9FTD/ALS. Neuron 2013;77:639-646.
Mori K, Weng SM, Arzberger T, et al. The C9orf72 GGGGCC repeat is translated into aggregating dipeptide-repeat proteins in FTLD/ALS. Science 2013;339:1335-1338.
MS and Salt?
Three studies published in the same issue of Nature describe some of the molecular routes to autoimmune diseases such as multiple sclerosis, and identify a diet high in salt as a potential risk factor for developing MS. TH17 is a type of T-cell that has been implicated in several autoimmune diseases. Mouse cells cultured in high-salt conditions produce more of these cells, and mice fed a high-salt diet develop a more severe form of an animal model for MS. While a high-salt diet is certainly not the only factor that leads someone to have MS, if this model is proven, a low-salt diet may be of benefit to those with the disease.
Sources:
Kleine-Wietfeld M, Manzel A, Titze J et al. Sodium chloride drives autoimmune disease by the induction of pathogenic TH17 cells. Nature 2013; 496(7446):518-522.
Wu C, Yosef N, Thalamhamer T et al. Induction of pathogenic TH17 cells by inducible salt-sensing kinase SGK1. Nature 2013: 496(7446)513-517.
Yosef N, Shalek AK, Gaublomme JT et al. Dynamic regulatory network controlling TH17 cell differentiation. Nature 2013 496(7446): 461-468.
Surgery for Intracranial Hemorrhage: Usually Not Worth It
Intracerebral hemorrhage may benefit from surgical evacuation, though generally the practice has been to leave them alone. The STICH II study suggests that in general surgery reduces mortality and leads to improved outcome in those with large hematomas whose brains were being compressed by the excess blood. The routine evacuation of intracerebral hematomas , however, is not advisable.
Source:
Mendelow AD, Gregson BA, Rowan EN, Murray GD, Gholkar A, Mitchell PM. Early surgery versus initial conservative treatment in patients with spontaneous supratentorial lobar intracerebral haematomas (STICH II): a randomised trial. Lancet 2013;382:397-408.
Vascular Disease and Dementia
Diseases such as Alzheimer’s disease have frequently been noted to go hand in hand with problems with blood vessels in the brain. This is important, because vascular disease is treatable, and doing so could significantly delay or decrease the severity of dementia. Delaying the onset of AD by one year would cut the prevalence by 20 percent, and delaying it by five years would cut the prevalence in half.
Source:
Toledo JB, Arnold SE, Raible K, et al. Contribution of cerebrovascular disease in autopsy confirmed neurodegenerative disease cases in the National Alzheimer's Coordinating Centre. Brain : a journal of neurology 2013;136:2697-2706.
Forecasting the Brain’s Lightning Storms
This study evaluated a system using an implanted device to provide patients with real time information about whether they were at risk for a seizure in the next half hour. This proves that reliable seizure prediction is feasible, as is recording of sub-clinical seizures that might suggest the need for better treatment.
Source:
Cook MJ, O'Brien TJ, Berkovic SF, et al. Prediction of seizure likelihood with a long-term, implanted seizure advisory system in patients with drug-resistant epilepsy: a first-in-man study. Lancet Neurology 2013;12:563-571.
A Diabetes Pill for Parkinson’s Disease?
This study provided early evidence that a drug usually used in diabetes is possibly effective in treating Parkinson’s as well. If true, this drug could quickly be repurposed towards treating Parkinson’s rather than waiting years to accumulate safety and tolerability data. With luck, this may spur on a more definitive phase 3 clinical trial.
Source:
Aviles-Olmos I, Dickson J, Kefalopoulou Z, et al. Exenatide and the treatment of patients with Parkinson's disease. The Journal of clinical investigation 2013;123:2730-2736.
There are certainly more, equally worthy publications that could be included in this by-no-means definitive list. That said, this should give some sense of the rapidly developing world of neuroscience. Here's looking forward to what 2014 has to bring!
Source:
The Neurology Today Editorial Advisory Board. Best Advances of 2013: Picks from the Neurology Today Editorial Advisory Board, Neurology Today: 19 December 2013 - Volume 13 - Issue 24 - pp 1,12,37–37
Written or reviewed by a board-certified physician. See About.com's Medical Review Board.
Every year the Editorial Advisory Board selects some of that year’s best scientific publications in the field of neuroscience. A “best-of” list is clearly a matter of some personal opinion, and cannot be considered complete, so I don't feel too bad about altering that list somewhat with some other selections of advances in neuroscience that made the news in 2013. Due to the ever-changing nature of science, is entirely possible that some of the selections will turn out to be not very important after all, while an overlooked publication will turn out to have huge implications in the future.
Caveats aside, here’s some of 2013’s neuroscientific highlights, in no particular order.
Sleep and the Brain’s Garbage Disposal
Why sleep is so important that we spend a third or so of our lives unconscious has been a major medical mystery. In 2012 the laboratory of Maiken Nedergaard described (and named) a glymphatic system that relies on cerebrospinal fluid to flush toxins such as beta-amyloid out of the brain. In 2013, the researchers discovered that the levels of toxins changed most while sleep. If this is accurate, we need to sleep so that our brains can take out the garbage.
Source:
Xie L, Kang H, Xu Q, Chen MJ, Liao Y, et al. Sleep Drives Metabolite Clearance from the Adult Brain. Science 18 October 2013: Vol. 342 no. 6156 pp. 373-377
Lab-Grown Mini-Brains…
Okay, really this is a model, but still, scientists used stem cells to create small and primitive versions of our own brains, with different cell types and firing neurons. While very far off from a full scale working human brain, this allows a new way to study diseases, especially of brain development.
Source:
Madeline A. Lancaster, Magdalena Renner, Carol-Anne Martin, et al. Cerebral organoids model human brain development and microcephaly. Nature, doi:10.1038/nature12517, epub Aug. 28
Move It or Lose It?
Need motivation to do more exercise? We’ve suspected for some time that physical exercise was one of the best ways to keep your brain sharp, but in 2013 researchers discovered one of the reasons why. A previously identified protein in muscles is increased in endurance exercise in the hippocampus of mice, and increases levels brain-derived neurotrophic factor (BDNF). BDNF is a substance that is also associated with better functioning of the hippocampus, responsible for learning and short-term memory.
Source:
Wrann CD, White JP, Salogiannis J, Laznik-Bogoslavski D, Wu J, et al. Exercise Induces Hippocampal BDNF through a PGC-1a/FNDC5 Pathway Cell Metabolism, Volume 18, Issue 5, 649-659, 10 October 2013
No Benefit to IA tPA Over tPA Alone in Acute Stroke
This paper demonstrated that additional treatment with endovascular treatments with intra-arterial tissue plasminogen activator tPA for ischemic stroke after tPA was administered intravenously did not have any benefit over giving tPA alone. What this means for other endovascular procedures for acute stroke, such as those using stent retrievers remain to be worked out.
Source:
Broderick JP, Palesch YY, Demchuk AM et al. Interventional Management of Stroke (IMS) III Investigators: Endovascular therapy after intravenous t-PA versus t-PA alone for stroke. N Engl J Med. 2013; 368(13): 1265.
An Insight into ALS and FTD
C9ORF72 has been tied with amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD). The gene consists of hundreds to thousands of GGGGCC repeats. These papers described how dipeptide proteins accumulate into inclusions as a result, providing some explanation for how the gene mutation causes these diseases.
Sources:
Ash PE, Bieniek KF, Gendron TF, et al. Unconventional translation of C9ORF72 GGGGCC expansion generates insoluble polypeptides specific to c9FTD/ALS. Neuron 2013;77:639-646.
Mori K, Weng SM, Arzberger T, et al. The C9orf72 GGGGCC repeat is translated into aggregating dipeptide-repeat proteins in FTLD/ALS. Science 2013;339:1335-1338.
MS and Salt?
Three studies published in the same issue of Nature describe some of the molecular routes to autoimmune diseases such as multiple sclerosis, and identify a diet high in salt as a potential risk factor for developing MS. TH17 is a type of T-cell that has been implicated in several autoimmune diseases. Mouse cells cultured in high-salt conditions produce more of these cells, and mice fed a high-salt diet develop a more severe form of an animal model for MS. While a high-salt diet is certainly not the only factor that leads someone to have MS, if this model is proven, a low-salt diet may be of benefit to those with the disease.
Sources:
Kleine-Wietfeld M, Manzel A, Titze J et al. Sodium chloride drives autoimmune disease by the induction of pathogenic TH17 cells. Nature 2013; 496(7446):518-522.
Wu C, Yosef N, Thalamhamer T et al. Induction of pathogenic TH17 cells by inducible salt-sensing kinase SGK1. Nature 2013: 496(7446)513-517.
Yosef N, Shalek AK, Gaublomme JT et al. Dynamic regulatory network controlling TH17 cell differentiation. Nature 2013 496(7446): 461-468.
Surgery for Intracranial Hemorrhage: Usually Not Worth It
Intracerebral hemorrhage may benefit from surgical evacuation, though generally the practice has been to leave them alone. The STICH II study suggests that in general surgery reduces mortality and leads to improved outcome in those with large hematomas whose brains were being compressed by the excess blood. The routine evacuation of intracerebral hematomas , however, is not advisable.
Source:
Mendelow AD, Gregson BA, Rowan EN, Murray GD, Gholkar A, Mitchell PM. Early surgery versus initial conservative treatment in patients with spontaneous supratentorial lobar intracerebral haematomas (STICH II): a randomised trial. Lancet 2013;382:397-408.
Vascular Disease and Dementia
Diseases such as Alzheimer’s disease have frequently been noted to go hand in hand with problems with blood vessels in the brain. This is important, because vascular disease is treatable, and doing so could significantly delay or decrease the severity of dementia. Delaying the onset of AD by one year would cut the prevalence by 20 percent, and delaying it by five years would cut the prevalence in half.
Source:
Toledo JB, Arnold SE, Raible K, et al. Contribution of cerebrovascular disease in autopsy confirmed neurodegenerative disease cases in the National Alzheimer's Coordinating Centre. Brain : a journal of neurology 2013;136:2697-2706.
Forecasting the Brain’s Lightning Storms
This study evaluated a system using an implanted device to provide patients with real time information about whether they were at risk for a seizure in the next half hour. This proves that reliable seizure prediction is feasible, as is recording of sub-clinical seizures that might suggest the need for better treatment.
Source:
Cook MJ, O'Brien TJ, Berkovic SF, et al. Prediction of seizure likelihood with a long-term, implanted seizure advisory system in patients with drug-resistant epilepsy: a first-in-man study. Lancet Neurology 2013;12:563-571.
A Diabetes Pill for Parkinson’s Disease?
This study provided early evidence that a drug usually used in diabetes is possibly effective in treating Parkinson’s as well. If true, this drug could quickly be repurposed towards treating Parkinson’s rather than waiting years to accumulate safety and tolerability data. With luck, this may spur on a more definitive phase 3 clinical trial.
Source:
Aviles-Olmos I, Dickson J, Kefalopoulou Z, et al. Exenatide and the treatment of patients with Parkinson's disease. The Journal of clinical investigation 2013;123:2730-2736.
There are certainly more, equally worthy publications that could be included in this by-no-means definitive list. That said, this should give some sense of the rapidly developing world of neuroscience. Here's looking forward to what 2014 has to bring!
Source:
The Neurology Today Editorial Advisory Board. Best Advances of 2013: Picks from the Neurology Today Editorial Advisory Board, Neurology Today: 19 December 2013 - Volume 13 - Issue 24 - pp 1,12,37–37
