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donderdag 27 september 2018

Nature Neuroscience Contents: October 2018 Volume 21 Number 10

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TABLE OF CONTENTS

October 2018 Volume 21, Issue 10

Editorial
News & Views
Review Articles
Articles
Resources
Amendments & Corrections
 
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Nikon's new A1R HD25 confocal system features the largest field of view on the market, enabling you to capture twice the data in a single shot. Increase your imaging throughput and gain better statistics with A1R HD25. 

Learn more

 

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'Call for Submissions, Rising Star Award in Neurodegenerative Research'

The Mahoney Institute for Neurosciences (MINS) at the University of Pennsylvania announces an international call for submissions for the Rising Star Award in Neurodegenerative Research, honoring a young researcher with a USD 10,000 personal honorarium at the MINS 35th Annual Retreat and Symposium April 3, 2019. 

Mahoney Institute for Neurosciences (MINS)
 
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Meet the shortlist!

The shortlist for this year's Nature Research Awards for Inspiring Science and Innovating Science has been announced. These Awards showcase exceptional achievements of leading women in science and of those who have encouraged girls and women to engage with STEM subjects.

See more about our shortlisted nominees >

In partnership with The Estée Lauder Companies.
 
 

Editorial

 

Focus on neurodegenerative disease    p1293
doi:10.1038/s41593-018-0250-x

News & Views

 

Deconstructing the synapse    pp1294 - 1295
Jason D. Shepherd
doi:10.1038/s41593-018-0244-8

Double threat in striatal dopamine signaling    pp1296 - 1297
Cody A. Siciliano, Fergil Mills & Kay M. Tye
doi:10.1038/s41593-018-0243-9

Social subjective value in the primate midbrain    pp1298 - 1299
Olga Dal Monte, Siqi Fan & Steve W. C. Chang
doi:10.1038/s41593-018-0230-1

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Review Articles

 

Converging pathways in neurodegeneration, from genetics to mechanisms    pp1300 - 1309
Li Gan, Mark R. Cookson, Leonard Petrucelli & Albert R. La Spada
doi:10.1038/s41593-018-0237-7

Neurodegenerative diseases cause progressive loss of brain functions associated with aging. Here we review intricate genotype–phenotype relationships, shared pathogenic mechanisms, and emerging therapeutic opportunities and challenges.

 

Deconstructing and targeting the genomic architecture of human neurodegeneration    pp1310 - 1317
Philip L. De Jager, Hyun-Sik Yang & David A Bennett
doi:10.1038/s41593-018-0240-z

Older people often have more than one form of neuropathology. The authors describe how insights from the genomic architecture of syndromically defined neurodegenerative diseases can be integrated to inform person-specific trajectories of brain aging.

 

The role of brain vasculature in neurodegenerative disorders    pp1318 - 1331
Melanie D. Sweeney, Kassandra Kisler, Axel Montagne, Arthur W. Toga & Berislav V. Zlokovic
doi:10.1038/s41593-018-0234-x

Adequate blood supply and vascular integrity are key to normal brain functioning. Cerebral blood flow and blood–brain barrier disruption contribute to Alzheimer’s disease and other neurodegenerative disorders as reviewed in humans and animal models.

 

Protein misfolding, aggregation, and conformational strains in neurodegenerative diseases    pp1332 - 1340
Claudio Soto & Sandra Pritzkow
doi:10.1038/s41593-018-0235-9

A newly recognized process in neurodegenerative disease is accumulation of misfolded protein aggregates that self-replicate to spread damage between cells and tissues. This process has implications in designing strategies for treatment and diagnosis.

 

Propagation and spread of pathogenic protein assemblies in neurodegenerative diseases    pp1341 - 1349
Mathias Jucker & Lary C. Walker
doi:10.1038/s41593-018-0238-6

Many neurodegenerative diseases involve the seeded propagation and spread of abnormally shaped proteins within the nervous system. The resulting disease reflects the interaction between the misfolded proteins and the host milieu.

 

Selective vulnerability in neurodegenerative diseases    pp1350 - 1358
Hongjun Fu, John Hardy & Karen E. Duff
doi:10.1038/s41593-018-0221-2

Neurodegenerative diseases impact specific cell populations within the brain. However, not all cells within the population are impacted, a phenomenon called selective cellular vulnerability. The molecular basis of this vulnerability is discussed.

 

Microglia in neurodegeneration    pp1359 - 1369
Suzanne Hickman, Saef Izzy, Pritha Sen, Liza Morsett & Joseph El Khoury
doi:10.1038/s41593-018-0242-x

Microglia are the sentinels, housekeepers, and defenders of the brain. In this review we consider the immune checkpoints that control microglial functions and discuss how their imbalance and subsequent neuroinflammation leads to neurodegeneration.

 

Animal models of neurodegenerative diseases    pp1370 - 1379
Ted M. Dawson, Todd E. Golde & Clotilde Lagier-Tourenne
doi:10.1038/s41593-018-0236-8

The authors review the current state of rodent models for AD, PD, FTD, and ALS. Limitations and utility of current models, issues regarding translatability, and future directions for developing animal models of these human disorders are discussed.

 

Articles

 

CNS lymphatic drainage and neuroinflammation are regulated by meningeal lymphatic vasculature    pp1380 - 1391
Antoine Louveau, Jasmin Herz, Maria Nordheim Alme, Andrea Francesca Salvador, Michael Q. Dong et al.
doi:10.1038/s41593-018-0227-9

Louveau et al. demonstrate that meningeal lymphatics drain CSF-derived macromolecules and immune cells and play a key role in regulating neuroinflammation. Meningeal lymphatics may represent a new therapeutic target for multiple sclerosis.

 

Maladaptive cortical hyperactivity upon recovery from experimental autoimmune encephalomyelitis    pp1392 - 1403
Erik Ellwardt, Gautam Pramanik, Dirk Luchtman, Tanja Novkovic, Eduardo Rosales Jubal et al.
doi:10.1038/s41593-018-0193-2

The authors report TNFα-dependent hyperactivity in cortical microcircuits during remission in a mouse model of multiple sclerosis, a maladaptive response to the immune attack with behavioral changes.

 

Impaired perceptual learning in a mouse model of Fragile X syndrome is mediated by parvalbumin neuron dysfunction and is reversible    pp1404 - 1411
Anubhuti Goel, Daniel A. Cantu, Janna Guilfoyle, Gunvant R. Chaudhari, Aditi Newadkar et al.
doi:10.1038/s41593-018-0231-0

Goel et al found similar deficits in visual discrimination in humans and in a mouse model of FXS. In mice, a robust decrease in PV cell activity mediated this impairment, suggesting that manipulating inhibition may improve sensory processing in FXS.

 

Restoring wild-type-like CA1 network dynamics and behavior during adulthood in a mouse model of schizophrenia    pp1412 - 1420
Thomas Marissal, Rodrigo F. Salazar, Cristina Bertollini, Sophie Mutel, Mathias De Roo et al.
doi:10.1038/s41593-018-0225-y

The authors report that impaired hippocampal synchrony in a mouse model of schizophrenia is due to parvalbumin interneuron hypoexcitability. Rescuing interneuron excitability during adulthood restores wild-type-like network dynamics and behavior.

 

Dopamine neurons projecting to the posterior striatum reinforce avoidance of threatening stimuli    pp1421 - 1430
William Menegas, Korleki Akiti, Ryunosuke Amo, Naoshige Uchida & Mitsuko Watabe-Uchida
doi:10.1038/s41593-018-0222-1

Menegas et al. show that dopamine neurons projecting to the posterior striatum reinforce avoidance of threatening stimuli. Their results indicate that there are two axes of reinforcement learning using dopamine, the value axis and the threat axis.

 

Coordinated cerebellar climbing fiber activity signals learned sensorimotor predictions    pp1431 - 1441
William Heffley, Eun Young Song, Ziye Xu, Benjamin N. Taylor, Mary Anne Hughes et al.
doi:10.1038/s41593-018-0228-8

Cerebellar climbing fibers provide predictive, context-specific instructional signals that do not rely exclusively on motor errors to support learning of arbitrary sensorimotor associations.

 

Neural implementation of Bayesian inference in a sensorimotor behavior    pp1442 - 1451
Timothy R. Darlington, Jeffrey M. Beck & Stephen G. Lisberger
doi:10.1038/s41593-018-0233-y

Behavior is the result of a Bayesian computation that weights past experience and current sensory information by their reliabilities. Here single-neuron activity in eye movement cortex exemplifies how the brain implements a Bayesian computation.

 

Social reward monitoring and valuation in the macaque brain    pp1452 - 1462
Atsushi Noritake, Taihei Ninomiya & Masaki Isoda
doi:10.1038/s41593-018-0229-7

Applying a social Pavlovian conditioning procedure for macaques, this study shows that medial prefrontal neurons selectively monitor self-reward or other-reward information and that dopamine neurons integrate this information into subjective value.

 

Inhibitory connectivity defines the realm of excitatory plasticity    pp1463 - 1470
Gianluigi Mongillo, Simon Rumpel & Yonatan Loewenstein
doi:10.1038/s41593-018-0226-x

Mongillo et al. use theoretical modeling to link structure & activity in a cortical network. They find that activity patterns are predominantly controlled by inhibitory connections, making the network robust to ongoing changes in excitatory synapses.

 

Triple dissociation of attention and decision computations across prefrontal cortex    pp1471 - 1481
Laurence T. Hunt, W. M. Nishantha Malalasekera, Archy O. de Berker, Bruno Miranda, Simon F. Farmer et al.
doi:10.1038/s41593-018-0239-5

Hunt, Malalasekera et al. recorded populations of prefrontal neurons from monkeys performing a visual attention-guided-choice task. The results revealed that distinct computations in three PFC subregions as information was sampled guided the eventual decision.

 

Resources

 

Enhancers active in dopamine neurons are a primary link between genetic variation and neuropsychiatric disease    pp1482 - 1492
Xianjun Dong, Zhixiang Liao, David Gritsch, Yavor Hadzhiev, Yunfei Bai et al.
doi:10.1038/s41593-018-0223-0

The BRAINcode consortium found that tens of thousands of transcribed noncoding elements (TNEs) from the ‘dark matter’ of our genome are active in dopamine neurons. They may be linked to schizophrenia, Parkinson’s disease, and addiction.

 

Amendments & Corrections

 

Author Correction: Dopamine transients are sufficient and necessary for acquisition of model-based associations    p1493
Melissa J Sharpe, Chun Yun Chang, Melissa A Liu, Hannah M Batchelor, Lauren E Mueller et al.
doi:10.1038/s41593-018-0202-5

Author Correction: Synaptic N6-methyladenosine (m6A) epitranscriptome reveals functional partitioning of localized transcripts    p1493
Daria Merkurjev, Wan-Ting Hong, Kei Iida, Ikumi Oomoto, Belinda J. Goldie et al.
doi:10.1038/s41593-018-0219-9

Author Correction: Retrieval induces adaptive forgetting of competing memories via cortical pattern suppression    p1493
Maria Wimber, Arjen Alink, Ian Charest, Nikolaus Kriegeskorte & Michael C Anderson
doi:10.1038/s41593-018-0220-3

Publisher Correction: The C-terminal tails of endogenous GluA1 and GluA2 differentially contribute to hippocampal synaptic plasticity and learning    p1494
Zikai Zhou, An Liu, Shuting Xia, Celeste Leung, Junxia Qi et al.
doi:10.1038/s41593-018-0116-2

Publisher Correction: Inhibitory circuit gating of auditory critical-period plasticity    p1495
Anne E. Takesian, Luke J. Bogart, Jeff W. Lichtman & Takao K. Hensch
doi:10.1038/s41593-018-0161-x

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