Example of Molecular Neurobiology format
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Example of Molecular Neurobiology format Example of Molecular Neurobiology format Example of Molecular Neurobiology format Example of Molecular Neurobiology format Example of Molecular Neurobiology format Example of Molecular Neurobiology format Example of Molecular Neurobiology format Example of Molecular Neurobiology format Example of Molecular Neurobiology format Example of Molecular Neurobiology format Example of Molecular Neurobiology format Example of Molecular Neurobiology format Example of Molecular Neurobiology format Example of Molecular Neurobiology format Example of Molecular Neurobiology format Example of Molecular Neurobiology format Example of Molecular Neurobiology format Example of Molecular Neurobiology format Example of Molecular Neurobiology format Example of Molecular Neurobiology format Example of Molecular Neurobiology format Example of Molecular Neurobiology format
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Example of Molecular Neurobiology format Example of Molecular Neurobiology format Example of Molecular Neurobiology format Example of Molecular Neurobiology format Example of Molecular Neurobiology format Example of Molecular Neurobiology format Example of Molecular Neurobiology format Example of Molecular Neurobiology format Example of Molecular Neurobiology format Example of Molecular Neurobiology format Example of Molecular Neurobiology format Example of Molecular Neurobiology format Example of Molecular Neurobiology format Example of Molecular Neurobiology format Example of Molecular Neurobiology format Example of Molecular Neurobiology format Example of Molecular Neurobiology format Example of Molecular Neurobiology format Example of Molecular Neurobiology format Example of Molecular Neurobiology format Example of Molecular Neurobiology format Example of Molecular Neurobiology format
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open access Open Access ISSN: 8937648 e-ISSN: 15591182
recommended Recommended

Molecular Neurobiology — Template for authors

Publisher: Springer
Categories Rank Trend in last 3 yrs
Neurology #13 of 156 up up by 20 ranks
Cellular and Molecular Neuroscience #12 of 88 up up by 19 ranks
journal-quality-icon Journal quality:
High
calendar-icon Last 4 years overview: 2327 Published Papers | 22984 Citations
indexed-in-icon Indexed in: Scopus
last-updated-icon Last updated: 18/07/2020
Insights & related journals
General info
Top papers
Popular templates
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FAQ

Journal Performance & Insights

  • Impact Factor
  • CiteRatio
  • SJR
  • SNIP

Impact factor determines the importance of a journal by taking a measure of frequency with which the average article in a journal has been cited in a particular year.

4.5

2% from 2018

Impact factor for Molecular Neurobiology from 2016 - 2019
Year Value
2019 4.5
2018 4.586
2017 5.076
2016 6.19
graph view Graph view
table view Table view

insights Insights

  • Impact factor of this journal has decreased by 2% in last year.
  • This journal’s impact factor is in the top 10 percentile category.

CiteRatio is a measure of average citations received per peer-reviewed paper published in the journal.

9.9

18% from 2019

CiteRatio for Molecular Neurobiology from 2016 - 2020
Year Value
2020 9.9
2019 8.4
2018 6.9
2017 6.2
2016 6.1
graph view Graph view
table view Table view

insights Insights

  • CiteRatio of this journal has increased by 18% in last years.
  • This journal’s CiteRatio is in the top 10 percentile category.

SCImago Journal Rank (SJR) measures weighted citations received by the journal. Citation weighting depends on the categories and prestige of the citing journal.

1.569

6% from 2019

SJR for Molecular Neurobiology from 2016 - 2020
Year Value
2020 1.569
2019 1.482
2018 1.472
2017 1.614
2016 1.748
graph view Graph view
table view Table view

insights Insights

  • SJR of this journal has increased by 6% in last years.
  • This journal’s SJR is in the top 10 percentile category.

Source Normalized Impact per Paper (SNIP) measures actual citations received relative to citations expected for the journal's category.

1.158

4% from 2019

SNIP for Molecular Neurobiology from 2016 - 2020
Year Value
2020 1.158
2019 1.112
2018 1.065
2017 1.055
2016 1.058
graph view Graph view
table view Table view

insights Insights

  • SNIP of this journal has increased by 4% in last years.
  • This journal’s SNIP is in the top 10 percentile category.

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Molecular Neurobiology

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Springer

Molecular Neurobiology

Molecular Neurobiology is an exciting review journal for neuroscientists needing to stay in close touch with progress at the forefront of molecular brain research today. It is an especially important periodical for graduate students and "postdocs," specifically designed to syn...... Read More

Neuroscience

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Last updated on
18 Jul 2020
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ISSN
0893-7648
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Impact Factor
High - 1.272
i
Open Access
No
i
Sherpa RoMEO Archiving Policy
Green faq
i
Plagiarism Check
Available via Turnitin
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Endnote Style
Download Available
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Bibliography Name
SPBASIC
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Citation Type
Author Year
(Blonder et al, 1982)
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Bibliography Example
Beenakker CWJ (2006) Specular andreev reflection in graphene. Phys Rev Lett 97(6):067,007, URL 10.1103/PhysRevLett.97.067007

Top papers written in this journal

Journal Article DOI: 10.1007/BF02740621
The cellular and molecular basis of peripheral nerve regeneration.
Susan Y. Fu1, Tessa Gordon1
01 Feb 1997 - Molecular Neurobiology

Abstract:

Functional recovery from peripheral nerve injury and repair depends on a multitude of factors, both intrinsic and extrinsic to neurons. Neuronal survival after axotomy is a prerequisite for regeneration and is facilitated by an array of trophic factors from multiple sources, including neurotrophins, neuropoietic cytokines, in... Functional recovery from peripheral nerve injury and repair depends on a multitude of factors, both intrinsic and extrinsic to neurons. Neuronal survival after axotomy is a prerequisite for regeneration and is facilitated by an array of trophic factors from multiple sources, including neurotrophins, neuropoietic cytokines, insulin-like growth factors (IGFs), and glial-cell-line-derived neurotrophic factors (GDNFs). Axotomized neurons must switch from a transmitting mode to a growth mode and express growth-associated proteins, such as GAP-43, tubulin, and actin, as well as an array of novel neuropeptides and cytokines, all of which have the potential to promote axonal regeneration. Axonal sprouts must reach the distal nerve stump at a time when its growth support is optimal. Schwann cells in the distal stump undergo proliferation and phenotypical changes to prepare the local environment to be favorable for axonal regeneration. Schwann cells play an indispensable role in promoting regeneration by increasing their synthesis of surface cell adhesion molecules (CAMs), such as N-CAM, Ng-CAM/L1, N-cadherin, and L2/HNK-1, by elaborating basement membrane that contains many extracellular matrix proteins, such as laminin, fibronectin, and tenascin, and by producing many neurotrophic factors and their receptors. However, the growth support provided by the distal nerve stump and the capacity of the axotomized neurons to regenerate axons may not be sustained indefinitely. Axonal regenerations may be facilitated by new strategies that enhance the growth potential of neurons and optimize the growth support of the distal nerve stump in combination with prompt nerve repair. read more read less

Topics:

Peripheral nerve injury (65%)65% related to the paper, Nerve guidance conduit (63%)63% related to the paper, Neurotrophic factors (59%)59% related to the paper, Regeneration (biology) (56%)56% related to the paper, Neurotrophin (54%)54% related to the paper
1,089 Citations
Journal Article DOI: 10.1007/S12035-014-9070-5
Differential Roles of M1 and M2 Microglia in Neurodegenerative Diseases
Yu Tang1, Weidong Le2
01 Mar 2016 - Molecular Neurobiology

Abstract:

One of the most striking hallmarks shared by various neurodegenerative diseases, including Parkinson's disease, Alzheimer's disease (AD), and amyotrophic lateral sclerosis, is microglia-mediated neuroinflammation. Increasing evidence indicates that microglial activation in the central nervous system is heterogeneous, which ca... One of the most striking hallmarks shared by various neurodegenerative diseases, including Parkinson's disease, Alzheimer's disease (AD), and amyotrophic lateral sclerosis, is microglia-mediated neuroinflammation. Increasing evidence indicates that microglial activation in the central nervous system is heterogeneous, which can be categorized into two opposite types: M1 phenotype and M2 phenotype. Depending on the phenotypes activated, microglia can produce either cytotoxic or neuroprotective effects. In this review, we focus on the potential role of M1 and M2 microglia and the dynamic changes of M1/M2 phenotypes that are critically associated with the neurodegenerative diseases. Generally, M1 microglia predominate at the injury site at the end stage of disease, when the immunoresolution and repair process of M2 microglia are dampened. This phenotype transformation is very complicated in AD due to the phagocytosis of regionally distributed β-amyloid (Aβ) plaque and tangles that are released into the extracellular space. The endogenous stimuli including aggregated α-synuclein, mutated superoxide dismutase, Aβ, and tau oligomers exist in the milieu that may persistently activate M1 pro-inflammatory responses and finally lead to irreversible neuron loss. The changes of microglial phenotypes depend on the disease stages and severity; mastering the stage-specific switching of M1/M2 phenotypes within appropriate time windows may provide better therapeutic benefit. read more read less

Topics:

Neuroinflammation (61%)61% related to the paper, Microglia (53%)53% related to the paper, Neuroprotection (53%)53% related to the paper
880 Citations
Journal Article DOI: 10.1007/BF02780662
129/Ola mice carrying a null mutation in PrP that abolishes mRNA production are developmentally normal.
Jean Manson, Alan Richard Clarke1, Martin L. Hooper1, L Aitchison, I McConnell, J Hope
01 Apr 1994 - Molecular Neurobiology

Abstract:

The neural membrane glycoprotein PrP is implicated in the pathogenesis of the transmissible spongiform encephalopathies; however, the normal function of PrP and its precise role in disease are not understood. Recently, gene targeting has been used to produce mice withneo/PrP fusion transcripts, but no detectable PrP protein i... The neural membrane glycoprotein PrP is implicated in the pathogenesis of the transmissible spongiform encephalopathies; however, the normal function of PrP and its precise role in disease are not understood. Recently, gene targeting has been used to produce mice withneo/PrP fusion transcripts, but no detectable PrP protein in the brain (1). Here we report the use of a different targeting strategy, to produce inbred mice with a complete absence of both PrP protein and mRNA sequences. At 7 mo of age, these mice show no overt phenotypic abnormalities despite the normal high levels of expression of PrP during mouse development. The mice are being used in experiments designed to address the role of PrP in the pathogenesis of scrapie and the replication of infectivity. read more read less

Topics:

Scrapie (55%)55% related to the paper, Gene targeting (51%)51% related to the paper
553 Citations
Journal Article DOI: 10.1385/MN:24:1-3:107
Molecular mechanisms of glutamate receptor-mediated excitotoxic neuronal cell death.
Rita Sattler1, Michael Tymianski2
01 Aug 2001 - Molecular Neurobiology

Abstract:

Excitotoxicity is one of the most extensively studied processes of neuronal cell death, and plays an important role in many central nervous system (CNS) diseases, including CNS ischemia, trauma, and neurodegenerative disorders. First described by Olney, excitotoxicity was later characterized as an excessive synaptic release o... Excitotoxicity is one of the most extensively studied processes of neuronal cell death, and plays an important role in many central nervous system (CNS) diseases, including CNS ischemia, trauma, and neurodegenerative disorders. First described by Olney, excitotoxicity was later characterized as an excessive synaptic release of glutamate, which in turn activates postsynaptic glutamate receptors. While almost every glutamate receptor subtype has been implicated in mediating excitotoxic cell death, it is generally accepted that the N-methyl-D-aspartate (NMDA) subtypes play a major role, mainly owing to their high calcium (Ca2+) permeability. However, other glutamate receptor subtypes such as 2-amino-3-(3-hydroxy-5-methylisoxazol-4-yl) propionate (AMPA) or kainate receptors have also been attributed a critical role in mediating excitotoxic neuronal cell death. Although the molecular basis of glutamate toxicity is uncertain, there is general agreement that it is in large part Ca2+-dependent. The present review is aimed at summarizing the molecular mechanisms of NMDA receptor and AMPA/kainate receptor-mediated excitotoxic neuronal cell death. read more read less

Topics:

Excitotoxicity (68%)68% related to the paper, Kainate receptor (65%)65% related to the paper, AMPA receptor (65%)65% related to the paper, NMDA receptor (64%)64% related to the paper, Neuroprotection (64%)64% related to the paper
520 Citations
Journal Article DOI: 10.1007/BF02741459
The diversity of GABAA receptors. Pharmacological and electrophysiological properties of GABAA channel subtypes.
Wulf Hevers1, Hartmut Lüddens1
01 Aug 1998 - Molecular Neurobiology

Abstract:

The amino acid γ-aminobutyric-acid (GABA) prevails in the CNS as an inhibitory neurotrans-mitter that mediates most of its effects through fast GABA-gated Cl−-channels (GABAAR). Molecular biology uncovered the complex subunit architecture of this receptor channel, in which a pentameric assembly derived from five of at least 1... The amino acid γ-aminobutyric-acid (GABA) prevails in the CNS as an inhibitory neurotrans-mitter that mediates most of its effects through fast GABA-gated Cl−-channels (GABAAR). Molecular biology uncovered the complex subunit architecture of this receptor channel, in which a pentameric assembly derived from five of at least 17 mammalian subunits, grouped in the six classes α, β, γ, δ, e, and ρ, permits a vast number of putative receptor isoforms. The subunit composition of a particular receptor determines the specific effects of allosterical modulators of the GABAARs like benzodiazepines (BZs), barbiturates, steroids, some convulsants, polyvalent cations, and ethanol. To understand the physiology and diversity of GABAARs, the native isoforms have to be identified by their localization in the brain and by their pharmacology. In heterologous expression systems, channels require the presence of α, β, and γ subunits in order to mimic the full repertoire of native receptor responses to drugs, with the BZ pharmacology being determined by the particular α and γ subunit variants. Little is known about the functional properties of the β, δ, and e subunit classes and only a few receptor subtype-specific substances like loreclezole and furosemide are known that enable the identification of defined receptor subtypes. We will summarize the pharmacology of putative receptor isoforms and emphasize the characteristics of functional channels. Knowledge of the complex pharmacology of GABAARs might eventually enable site-directed drug design to further our understanding of GABA-related disorders and of the complex interaction of excitatory and inhibitory mechanisms in neuronal processing. read more read less

Topics:

GABAA-rho receptor (62%)62% related to the paper, GABAA receptor (56%)56% related to the paper, Loreclezole (56%)56% related to the paper, Receptor (53%)53% related to the paper, Protein subunit (52%)52% related to the paper
455 Citations
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Molecular Neurobiology format uses SPBASIC citation style.

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Frequently asked questions

Absolutely not! With our tool, you can freely write without having to focus on LaTeX. You can write your entire paper as per the Molecular Neurobiology guidelines and autoformat it.

Yes. The template is fully compliant as per the guidelines of this journal. Our experts at SciSpace ensure that. Also, if there's any update in the journal format guidelines, we take care of it and include that in our algorithm.

Sure. We support all the top citation styles like APA style, MLA style, Vancouver style, Harvard style, Chicago style, etc. For example, in case of this journal, when you write your paper and hit autoformat, it will automatically update your article as per the Molecular Neurobiology citation style.

You can avail our Free Trial for 7 days. I'm sure you'll find our features very helpful. Plus, it's quite inexpensive.

Yup. You can choose the right template, copy-paste the contents from the word doc and click on auto-format. You'll have a publish-ready paper that you can download at the end.

A matter of seconds. Besides that, our intuitive editor saves a load of your time in writing and formating your manuscript.

One little Google search can get you the Word template for any journal. However, why do you need a Word template when you can write your entire manuscript on SciSpace, autoformat it as per Molecular Neurobiology's guidelines and download the same in Word, PDF and LaTeX formats? Try us out!.

Absolutely! You can do it using our intuitive editor. It's very easy. If you need help, you can always contact our support team.

SciSpace is an online tool for now. We'll soon release a desktop version. You can also request (or upvote) any feature that you think might be helpful for you and the research community in the feature request section once you sign-up with us.

Sure. You can request any template and we'll have it up and running within a matter of 3 working days. You can find the request box in the Journal Gallery on the right sidebar under the heading, "Couldn't find the format you were looking for?".

After you have written and autoformatted your paper, you can download it in multiple formats, viz., PDF, Docx and LaTeX.

To be honest, the answer is NO. The impact factor is one of the many elements that determine the quality of a journal. Few of those factors the review board, rejection rates, frequency of inclusion in indexes, Eigenfactor, etc. You must assess all the factors and then take the final call.

SHERPA/RoMEO Database

We have extracted this data from Sherpa Romeo to help our researchers understand the access level of this journal. The following table indicates the level of access a journal has as per Sherpa Romeo Archiving Policy.

RoMEO Colour Archiving policy
Green Can archive pre-print and post-print or publisher's version/PDF
Blue Can archive post-print (ie final draft post-refereeing) or publisher's version/PDF
Yellow Can archive pre-print (ie pre-refereeing)
White Archiving not formally supported
FYI:
  1. Pre-prints as being the version of the paper before peer review and
  2. Post-prints as being the version of the paper after peer-review, with revisions having been made.

The 5 most common citation types in order of usage are:.

S. No. Citation Style Type
1. Author Year
2. Numbered
3. Numbered (Superscripted)
4. Author Year (Cited Pages)
5. Footnote

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After uploading your paper on SciSpace, you would see a button to request a journal submission service for Molecular Neurobiology.

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Yes. SciSpace provides this functionality.

After signing up, you would need to import your existing references from Word or .bib file.

SciSpace would allow download of your references in Molecular Neurobiology Endnote style, according to springer guidelines.

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