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
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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
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open access Open Access
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
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Related Journals

open access Open Access

Springer

Quality:  
High
CiteRatio: 6.0
SJR: 1.239
SNIP: 1.096
open access Open Access

Springer

Quality:  
High
CiteRatio: 6.8
SJR: 1.582
SNIP: 1.194
open access Open Access
recommended Recommended

Springer

Quality:  
High
CiteRatio: 10.1
SJR: 2.615
SNIP: 1.649
open access Open Access
recommended Recommended

Wiley

Quality:  
High
CiteRatio: 10.7
SJR: 2.954
SNIP: 1.449

Journal Performance & Insights

Impact Factor

CiteRatio

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.

A measure of average citations received per peer-reviewed paper published in the journal.

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

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

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

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)

Source Normalized Impact per Paper (SNIP)

Measures weighted citations received by the journal. Citation weighting depends on the categories and prestige of the citing journal.

Measures actual citations received relative to citations expected for the journal's category.

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

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

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

insights Insights

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

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
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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/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
1,319 Citations
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
1,126 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
565 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
539 Citations
open accessOpen access Journal Article DOI: 10.1007/S12035-012-8344-Z
Molecular Mechanisms of Ischemia–Reperfusion Injury in Brain: Pivotal Role of the Mitochondrial Membrane Potential in Reactive Oxygen Species Generation
Thomas H. Sanderson1, Christian A. Reynolds1, Rita Kumar1, Karin Przyklenk1, Maik Hüttemann1
01 Feb 2013 - Molecular Neurobiology

Abstract:

Stroke and circulatory arrest cause interferences in blood flow to the brain that result in considerable tissue damage. The primary method to reduce or prevent neurologic damage to patients suffering from brain ischemia is prompt restoration of blood flow to the ischemic tissue. However, paradoxically, restoration of blood fl... Stroke and circulatory arrest cause interferences in blood flow to the brain that result in considerable tissue damage. The primary method to reduce or prevent neurologic damage to patients suffering from brain ischemia is prompt restoration of blood flow to the ischemic tissue. However, paradoxically, restoration of blood flow causes additional damage and exacerbates neurocognitive deficits among patients who suffer a brain ischemic event. Mitochondria play a critical role in reperfusion injury by producing excessive reactive oxygen species (ROS) thereby damaging cellular components, and initiating cell death. In this review, we summarize our current understanding of the mechanisms of mitochondrial ROS generation during reperfusion, and specifically, the role the mitochondrial membrane potential plays in the pathology of cerebral ischemia/reperfusion. Additionally, we propose a temporal model of ROS generation in which posttranslational modifications of key oxidative phosphorylation (OxPhos) proteins caused by ischemia induce a hyperactive state upon reintroduction of oxygen. Hyperactive OxPhos generates high mitochondrial membrane potentials, a condition known to generate excessive ROS. Such a state would lead to a “burst” of ROS upon reperfusion, thereby causing structural and functional damage to the mitochondria and inducing cell death signaling that eventually culminate in tissue damage. Finally, we propose that strategies aimed at modulating this maladaptive hyperpolarization of the mitochondrial membrane potential may be a novel therapeutic intervention and present specific studies demonstrating the cytoprotective effect of this treatment modality. read more read less

Topics:

Mitochondrial ROS (63%)63% related to the paper, Reperfusion injury (63%)63% related to the paper, Ischemia (57%)57% related to the paper, Brain ischemia (56%)56% related to the paper, Inner mitochondrial membrane (54%)54% related to the paper
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521 Citations
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Molecular Neurobiology format uses SPBASIC citation style.

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Frequently asked questions

1. Can I write Molecular Neurobiology in LaTeX?

Absolutely not! Our tool has been designed to help you focus on writing. You can write your entire paper as per the Molecular Neurobiology guidelines and auto format it.

2. Do you follow the Molecular Neurobiology guidelines?

Yes, the template is compliant with the Molecular Neurobiology guidelines. Our experts at SciSpace ensure that. If there are any changes to the journal's guidelines, we'll change our algorithm accordingly.

3. Can I cite my article in multiple styles in Molecular Neurobiology?

Of course! We support all the top citation styles, such as APA style, MLA style, Vancouver style, Harvard style, and Chicago style. For example, when you write your paper and hit autoformat, our system will automatically update your article as per the Molecular Neurobiology citation style.

4. Can I use the Molecular Neurobiology templates for free?

Sign up for our free trial, and you'll be able to use all our features for seven days. You'll see how helpful they are and how inexpensive they are compared to other options, Especially for Molecular Neurobiology.

5. Can I use a manuscript in Molecular Neurobiology that I have written in MS Word?

Yes. You can choose the right template, copy-paste the contents from the word document, and click on auto-format. Once you're done, you'll have a publish-ready paper Molecular Neurobiology that you can download at the end.

6. How long does it usually take you to format my papers in Molecular Neurobiology?

It only takes a matter of seconds to edit your manuscript. Besides that, our intuitive editor saves you from writing and formatting it in Molecular Neurobiology.

7. Where can I find the template for the Molecular Neurobiology?

It is possible to find the Word template for any journal on Google. However, why use a template when you can write your entire manuscript on SciSpace , auto format it as per Molecular Neurobiology's guidelines and download the same in Word, PDF and LaTeX formats? Give us a try!.

8. Can I reformat my paper to fit the Molecular Neurobiology's guidelines?

Of course! You can do this using our intuitive editor. It's very easy. If you need help, our support team is always ready to assist you.

9. Molecular Neurobiology an online tool or is there a desktop version?

SciSpace's Molecular Neurobiology is currently available as an online tool. We're developing a desktop version, too. You can request (or upvote) any features that you think would be helpful for you and other researchers in the "feature request" section of your account once you've signed up with us.

10. I cannot find my template in your gallery. Can you create it for me like Molecular Neurobiology?

Sure. You can request any template and we'll have it setup within a few days. You can find the request box in Journal Gallery on the right side bar under the heading, "Couldn't find the format you were looking for like Molecular Neurobiology?”

11. What is the output that I would get after using Molecular Neurobiology?

After writing your paper autoformatting in Molecular Neurobiology, you can download it in multiple formats, viz., PDF, Docx, and LaTeX.

12. Is Molecular Neurobiology's impact factor high enough that I should try publishing my article there?

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 these factors include review board, rejection rates, frequency of inclusion in indexes, and Eigenfactor. You need to assess all these factors before you make your final call.

13. What is Sherpa RoMEO Archiving Policy for Molecular Neurobiology?

SHERPA/RoMEO Database

We extracted this data from Sherpa Romeo to help researchers understand the access level of this journal in accordance with the Sherpa Romeo Archiving Policy for Molecular Neurobiology. The table below indicates the level of access a journal has as per Sherpa Romeo's 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.

14. What are the most common citation types In Molecular Neurobiology?

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

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

15. How do I submit my article to the Molecular Neurobiology?

It is possible to find the Word template for any journal on Google. However, why use a template when you can write your entire manuscript on SciSpace , auto format it as per Molecular Neurobiology's guidelines and download the same in Word, PDF and LaTeX formats? Give us a try!.

16. Can I download Molecular Neurobiology in Endnote format?

Yes, SciSpace provides this functionality. After signing up, you would need to import your existing references from Word or Bib file to SciSpace. Then SciSpace would allow you to download your references in Molecular Neurobiology Endnote style according to Elsevier guidelines.

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