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Top Neuroscience Discoveries of 2016


mbeyeler

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As the year comes to a close, I thought it would be interesting to look back and identify some of the most influential, memorable, or surprising findings that neuroscience had to offer in 2016.

Here are some of my favorites:

Humans aren’t the only great apes that can “read minds”: In an ingenious experiment involving video and a man in an ape suit, researchers showed this year that apes understand when another ape holds a false belief, which is believed to underlie deception, empathy, teaching, and perhaps even language. The groundbreaking study suggests that this skill likely can be traced back to the last common ancestor of great apes and humans, and may be found in other species.

Transplanted embryonic neurons integrate into adult neocortical circuits: Researchers at the Max Planck Institute of Neurobiology in Martinsried, the Ludwig Maximilians University Munich and the Helmholtz Zentrum Munich have demonstrated that, in mice, transplanted embryonic nerve cells can be incorporated into an existing network and correctly carry out the tasks of damaged cells originally found in that region.
http://dx.doi.org/10.1038/nature20113

3D mapping of the mouse cortex: Researchers from the Allen Institute for Brain Science have completed the 3D mapping of the mouse cortex as part of the Allen Mouse Common Coordinate Framework (CCF): a standardized spatial coordinate system for comparing many types of data on the brain from the suite of Allen Brain Atlas resources.
https://www.alleninstitute.org/

Human eye spots single photons: Human eyes are capable of detecting a single photon—the tiniest possible speck of light—researchers from the Rockefeller University have found. They also found that the human eye is more sensitive to single photons shortly after it has seen another photon.

The root of all evil: Dr. Dayu Lin and colleagues from the NYU Langone Medical Center have uncovered a distinct part of the brain that fires up right before premeditated nefarious acts are carried out.

New Alzheimer’s treatment fully restores memory function: Australian researchers have come up with a noninvasive ultrasound technology that clears the brain of neurotoxic amyloid plaques—structures that are responsible for memory loss and a decline in cognitive function in Alzheimer’s patients. The team reports fully restoring the memory function of 75 percent of the mice they tested it on, with zero damage to the surrounding brain tissue.

Live long and prosper: In several studies this year, researchers showed that eliminating worn-out cells helps mice live longer, healthier lives, and seems to stave off a multitude of age-related diseases. We might eventually enjoy the same benefits, with the launch today of a company aiming to develop drugs that wipe out these “senescent” cells in humans.

Anything else come to mind? What are your favorite findings of 2016?

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  • 2 weeks later...

Fully agree with your selections and are here are mine:
In view of research we performed in the 90s showing that microglial antibodies in the cerebrospinal fluid of Alzheimer’s disease patients had the potential to be biomarkers I am always very pleased that microglia associated with Alzheimer’s disease remain as a potential biomarkers
In March 2016 Researchers at the Ludwig-Maximilians-University, the German Center for Neurodegenerative Diseases (DZNE), and the Institute for Stroke and Dementia Research (ISD) in Munich, Germany, identified a brain inflammation marker in patients at early asymptomatic stages of Alzheimer’s disease. This secreted marker molecule, which can be measured from cerebrospinal fluid taps, may provide clinicians with a rapidly detectable biomarker for the transition from preclinical Alzheimer’s disease to cognitive impairment and progression to full dementia
Suárez-Calvet M et al., TREM2 cerebrospinal fluid levels are a potential biomarker for microglia activity in early-stage Alzheimer’s Disease and associate with neuronal injury markers, EMBO Molecular Medicine (2016). doi: 10.15252/emmm.201506123

Research linking gut microbiota to neurodegenerative disorders are very interesting and provide new avenues for models and therapeutics. Both Parkinson and Alzheimer’s disease have been explored.
1. PARKINSON’S DISEASE
Gut Microbiota Regulate Motor Deficits and Neuroinflammation in a Model of Parkinson’s DiseaseTimothy R. Sampson et al Department of Neurology, University of Wisconsin-Madison, Madison, WI 53705, USA**
According to the authors: The intestinal microbiota influence neurodevelopment, modulate behavior, and contribute to neurological disorders. However, a functional link between gut bacteria and neurodegenerative diseases remains unexplored. Synucleinopathies are characterized by aggregation of the protein α-synuclein (αSyn), often resulting in motor dysfunction as exemplified by Parkinson’s disease (PD). Using mice that overexpress αSyn, we report herein that gut microbiota are required for motor deficits, microglia activation, and αSyn pathology. Antibiotic treatment ameliorates, while microbial re-colonization promotes, pathophysiology in adult animals, suggesting that postnatal signaling between the gut and the brain modulates disease
2. ALZHEIMER’S DISEASE
Chen, S. G. et al. Exposure to the Functional Bacterial Amyloid Protein Curli Enhances Alpha-Synuclein Aggregation in Aged Fischer 344 Rats and Caenorhabditis elegans. Sci. Rep. 6, 34477; doi: 10.1038/srep34477 (2016) Dept. of Neurology, University of Louisville School of Medicine, Louisville, Kentucky, USA
Briefly their study showed that rats exposed to E. coli producing the extracellular bacterial amyloid protein curli displayed increased neuronal alpha-synuclein deposition in both gut and brain and enhanced microgliosis and astrogliosis compared to rats exposed to either mutant bacteria unable to synthesize curli, or to vehicle alone. Their concluded that amyloid proteins in the microbiota are involved in the origination and maintenance of neurodegenerative disease.

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Great selections so far!

One of the most memorable findings for me was the idea that astrocyte mitochondria could be taken up and used by neurons as a possible defense against cell death in stroke (http://www.nature.com/nature/journal/v535/n7613/full/nature18928.html)

While it wouldn’t be fair for me to post this without also listing the alternative argument (http://www.sciencedirect.com/science/article/pii/S1550413116304405), it is nonetheless an exciting concept that may alter current perceptions of cross-talk between neurons and glia.

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