Neuroscience & Biobehavioral Reviews (NEUROSCI BIOBEHAV R)

Publisher: Elsevier

Journal description

The journal will publish original and significant review articles dealing with all aspects of neuroscience, where the relationship to the study of psychological processes and behavior is clearly established. Conversely, the journal will also publish articles whose primary focus deals with psychological processes and behavior, and which have relevance to one or more aspects of neuroscience. Submissions to the journal are actively encouraged which deal with topics not only in the more traditional areas, but also in the following areas, whenever the reviews bring new insights into brain-behavior relations: neuropsychology cognitive neuroscience brain imaging in vivo monitoring of the brain's electrical and biochemical activities molecular biology genetics neurocomputation Theoretical articles and mini-reviews, for which the scope and literature coverage are more restricted, will also be published. The table of contents for this journal is now available pre-publication, via e-mail, as part of the free ContentsDirect service from Elsevier Science. Please send an e-mail message to for further information about this service.

Current impact factor: 8.80

Impact Factor Rankings

2015 Impact Factor Available summer 2016
2014 Impact Factor 8.802
2013 Impact Factor 10.284
2012 Impact Factor 9.44
2011 Impact Factor 8.65
2010 Impact Factor 9.015
2009 Impact Factor 7.791
2008 Impact Factor 7.804
2007 Impact Factor 8.147
2006 Impact Factor 8.293
2005 Impact Factor 7.443
2004 Impact Factor 6.346
2003 Impact Factor 5.482
2002 Impact Factor 5.504
2001 Impact Factor 5.212
2000 Impact Factor 3.382
1999 Impact Factor 3.595
1998 Impact Factor 3.316
1997 Impact Factor 2.786

Impact factor over time

Impact factor

Additional details

5-year impact 10.53
Cited half-life 6.40
Immediacy index 1.66
Eigenfactor 0.04
Article influence 3.59
Website Neuroscience & Biobehavioral Reviews website
Other titles Neuroscience and biobehavioral reviews, Neuroscience & biobehavioral reviews
ISSN 1873-7528
OCLC 3552135
Material type Periodical, Internet resource
Document type Journal / Magazine / Newspaper, Internet Resource

Publisher details


  • Pre-print
    • Author can archive a pre-print version
  • Post-print
    • Author can archive a post-print version
  • Conditions
    • Authors pre-print on any website, including arXiv and RePEC
    • Author's post-print on author's personal website immediately
    • Author's post-print on open access repository after an embargo period of between 12 months and 48 months
    • Permitted deposit due to Funding Body, Institutional and Governmental policy or mandate, may be required to comply with embargo periods of 12 months to 48 months
    • Author's post-print may be used to update arXiv and RepEC
    • Publisher's version/PDF cannot be used
    • Must link to publisher version with DOI
    • Author's post-print must be released with a Creative Commons Attribution Non-Commercial No Derivatives License
    • Publisher last reviewed on 03/06/2015
  • Classification

Publications in this journal

  • [Show abstract] [Hide abstract]
    ABSTRACT: Though numerous studies have implicated structural abnormalities in chronically depressive patients, relatively little attention has been paid to the brain alterations in patients experiencing first episode depression (FED). The investigation of FED is important for elucidating the core pathophysiology of this disease independent of other potentially confounding factors. The present study was to provide a quantitative voxelwise meta-analysis of grey matter (GM) changes in FED using effect-size signed differential mapping (ES-SDM). The pooled meta-analysis revealed GM reductions in the right supplementary motor area, left insula, and right middle temporal gyrus in FED patients compared with the healthy controls. No GM volume increases were found. The meta-regression analyses showed that studies including patients with higher HDRS scores were significantly more likely to present reduced GM volumes in the right amygdala. This meta-analysis indicates that FED patients have significantly and robustly reduced grey matter mainly associated with emotion regulation and sensorimotor areas alterations may be specific changes in early stage of this disease.
    Neuroscience & Biobehavioral Reviews 11/2015; DOI:10.1016/j.neubiorev.2015.10.011
  • [Show abstract] [Hide abstract]
    ABSTRACT: RAYNER, G., G. Jackson and S. Wilson. Cognition-related brain networks underpin the symptomotology of unipolar depression: evidence from a systematic review. NEUROSCI BIOBEHAV REV XXX-XXX, 2015.- This systematic review sources the latest neuroimaging evidence for the role of cognition-related brain networks in depression, and relates their abnormal functioning to symptoms of the disorder. Using theoretically informed and rigorous inclusion criteria, we integrate findings from 59 functional neuroimaging studies of adults with unipolar depression using a narrative approach. Results demonstrate that two distinct neurocognitive networks, the autobiographic memory network (AMN) and the cognitive control network (CCN), are central to the symptomotology of depression. Specifically, hyperactivity of the introspective AMN is linked to pathological brooding, self-blame, rumination. Anticorrelated under-engagement of the CCN is associated with indecisiveness, negative automatic thoughts, poor concentration, distorted cognitive processing. Downstream effects of this imbalance include reduced regulation of networks linked to the vegetative and affective symptoms of depression. The configurations of these networks can change between individuals and over time, plausibly accounting for both the variable presentation of depressive disorders and their fluctuating course. Framing depression as a disorder of neurocognitive networks directly links neurobiology to psychiatric practice, aiding researchers and clinicians alike.
    Neuroscience & Biobehavioral Reviews 11/2015; DOI:10.1016/j.neubiorev.2015.09.022
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    ABSTRACT: Studies have demonstrated that aerobic exercise can enhance insulin sensitivity, however, the precise mechanism for this outcome is not entirely identified. Emerging evidences point out that exercise can upregulate galanin protein and mRNA expression, resulting in improvement of insulin sensitivity via an increase in translocation of glucose transporter 4 and subsequent glucose uptake in myocytes and adipocytes of healthy and type 2 diabetic rats, which may be blocked by galanin antagonist. In return, galanin can exert the exercise-protective roles to prevent excessive movement of skeletal muscle and to accelerate exercise trauma repair in exercise-relative tissues. Studies also implicated that combination of aerobic exercise and activation of galanin system may make more significant improvement in insulin sensitivity than that of either one did. These suggest that galanin system is essential for physical activity to alleviate insulin resistance, namely, the beneficial effect of physical activity on glucose uptake is at least partly mediated by galanin system. Besides, co-treatment with galanin and exercise is an effective therapeutic strategy for reducing insulin resistance.
    Neuroscience & Biobehavioral Reviews 11/2015; 59. DOI:10.1016/j.neubiorev.2015.09.012
  • M. Boccia · S. Barbetti · L. Piccardi · C. Guariglia · F. Ferlazzo · A.M. Giannini · D.W. Zaidel ·

    Neuroscience & Biobehavioral Reviews 11/2015; DOI:10.1016/j.neubiorev.2015.09.009
  • Sen Cheng · Markus Werning · Thomas Suddendorf ·

    Neuroscience & Biobehavioral Reviews 11/2015; DOI:10.1016/j.neubiorev.2015.11.011
  • [Show abstract] [Hide abstract]
    ABSTRACT: Amyotrophic lateral sclerosis (ALS) is now recognized as a multisystem disorder, in which the primary pathology is the degeneration of motor neurons, with cognitive and/or behavioral dysfunctions that constitutes the non-motor manifestations of ALS. The combination of clinical, neuroimaging, and neuropathological data, and detailed genetic studies suggest that ALS and frontotemporal dementia (FTD) might form part of a disease continuum, with pure ALS and pure FTD at the two extremes. Mutations in the superoxide dismutase 1 (SOD1) gene were the first genetic mutations linked to the insurgence of ALS. Since that discovery numerous animal models carrying SOD1 mutations have been created. Despite their limitations these animal models, particularly the mice, have broaden our knowledge on the system alterations occurring in the ALS spectrum of disorders. The present review aims at providing an overview of the data obtained with the SOD1 animal models first and foremost on the cortical and subcortical regions, the cortico-striatal and hippocampal synaptic plasticity, dendritic branching and glutamate receptors function.
    Neuroscience & Biobehavioral Reviews 11/2015; DOI:10.1016/j.neubiorev.2015.11.006
  • Marietta Papadatou-Pastou · Anna Sáfár ·

    Neuroscience & Biobehavioral Reviews 11/2015; DOI:10.1016/j.neubiorev.2015.11.013
  • [Show abstract] [Hide abstract]
    ABSTRACT: The gene coding for the dopamine transporter (DAT), SLC6A3, contains a 40-base pair variable number of tandem repeats (VNTR) polymorphism (rs28363170) in its 3' untranslated region. This VNTR has been associated with attention deficit hyperactivity disorder (ADHD) and has been investigated in relation to cognition and brain function. Here, we report the results of a comprehensive meta-analysis with meta-regression examining the association of the VNTR with different domains of cognition in healthy adults. We extracted data from 28 independent studies and carried out meta-analyses for associations with working memory (k=10 samples, N=1193 subjects), inhibition (k=8 samples, N=829 subjects), executive functions including inhibition (k=10 samples, N=984 subjects), attention (k=6 samples, N=742 subjects) and declarative long-term memory (k=5 samples, N=251 subjects). None of the investigated dimensions showed significant associations with the VNTR (all p>0.26). Meta-regression including year of publication, gender, age, ethnicity and percentage of 10R-homozygotes similarly did not attain significance. We conclude that there is no evidence that rs28363170 may be a significant predictor of cognitive function in healthy adults.
    Neuroscience & Biobehavioral Reviews 11/2015; DOI:10.1016/j.neubiorev.2015.09.021
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    ABSTRACT: NEUROSCI BIOBEHAV REV.- The discovery of microRNAs (miRNAs) a little over 20 years ago was revolutionary given that miRNAs are essential to numerous physiological and physiopathological processes. Currently, several aspects of the biogenic process of miRNAs and of the translational repression mechanism exerted on their targets mRNAs are known in detail. In fact, the development of bioinformatics tools for predicting miRNA targets has established that miRNAs have the potential to regulate almost all known biological processes. Therefore, the identification of the signals and molecular mechanisms that regulate miRNA function is relevant to understanding the role of miRNAs in both pathological and adaptive processes. Recently, a series of studies has focused on miRNA expression in the brain, establishing that their levels are altered in response to various environmental factors (EFs), such as light, sound, odorants, nutrients, drugs and stress. In this review, we discuss how exposure to various EFs modulates the expression and function of several miRNAs in the nervous system and how this control determines adaptation to their environment, behavior and disease state.
    Neuroscience & Biobehavioral Reviews 11/2015; DOI:10.1016/j.neubiorev.2015.10.010

  • Neuroscience & Biobehavioral Reviews 11/2015; DOI:10.1016/j.neubiorev.2015.11.008

  • Neuroscience & Biobehavioral Reviews 11/2015; DOI:10.1016/j.neubiorev.2015.11.007
  • [Show abstract] [Hide abstract]
    ABSTRACT: Addiction involves alterations in multiple brain regions that are associated with functions such as memory, motivation and executive control. Indeed, it is now well accepted that addictive drugs produce long-lasting molecular and structural plasticity changes in corticostriatal-limbic loops. However, there are brain regions that might be relevant to addiction other than the prefrontal cortex, amygdala, hippocampus and basal ganglia. In addition to these circuits, a growing amount of data suggests the involvement of the cerebellum in many of the brain functions affected in addicts, though this region has been overlooked, traditionally, in the addiction field. Therefore, in the present review we provide seven arguments as to why we should consider the cerebellum in drug addiction. We present and discuss compelling evidence about the effects of drugs of abuse on cerebellar plasticity, the involvement of the cerebellum in drug-induced cue-related memories, and several findings showing that the instrumental memory and executive functions also recruit the cerebellar circuitry. In addition, a hypothetical model of the cerebellum's role relative to other areas within the corticostriatal-limbic circuitry is also provided. Our goal is not to review animal and human studies exhaustively but to support the inclusion of cerebellar alterations as a part of the physiopathology of addiction disorder.
    Neuroscience & Biobehavioral Reviews 11/2015; DOI:10.1016/j.neubiorev.2015.11.005
  • [Show abstract] [Hide abstract]
    ABSTRACT: Cognitive dysfunction is highly prevalent, disabling, and poorly-managed in persons with multiple sclerosis (MS). Exercise training represents a promising approach for managing this clinical symptom of the disease. However, results from early randomized controlled trials of exercise on cognition in MS are equivocal, perhaps due to methodological concerns. This underscores the importance of considering the well-established literature in the general population that documents robust, beneficial effects of exercise training on cognition across the lifespan. The development of such successful interventions is based on examinations of fitness, physical activity, and acute exercise effects on cognition. Applying such an evidence-based approach in MS serves as a way of better informing exercise training interventions for improving cognition in this population. To that end, this paper provides a focused, updated review on the evidence describing exercise effects on cognition in MS, and develops a rationale and framework for examining acute exercise on cognitive outcomes in this population. This will provide keen insight for better developing exercise interventions for managing cognitive impairment in MS.
    Neuroscience & Biobehavioral Reviews 11/2015; DOI:10.1016/j.neubiorev.2015.10.012
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    ABSTRACT: Compelling evidence suggests that fear generalization (i.e. the transfer of fear from a particular stimulus to another one sharing similarities with the original stimulus) may contribute to the development of posttraumatic stress disorder (PTSD), for which current treatments are ineffective. Deficits in hippocampus-mediated pattern separation, the process by which memories are stored as unique representations that are resistant to confusion, have been solely proposed as a putative underlying marker of generalization. We delineate instead an enlarged scenario, wherein conditioned and generalized fear memories share a common neurocircuitry, with the hippocampus being the nub of contextual fear, and the prefrontal cortex of both cued and contextual fear. The potential contribution of the amygdala and insula will be highlighted as well. Finally, we will consider vulnerability factors that may contribute to the development of PTSD, and suggest avenues for novel therapeutics. A better understanding of the mechanisms behind fear generalization is fundamental to provide further insight into treatment of debilitating conditions such as PTSD.
    Neuroscience & Biobehavioral Reviews 10/2015; DOI:10.1016/j.neubiorev.2015.10.009