Example of Journal of Molecular Neuroscience format
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Example of Journal of Molecular Neuroscience format Example of Journal of Molecular Neuroscience format Example of Journal of Molecular Neuroscience format Example of Journal of Molecular Neuroscience format Example of Journal of Molecular Neuroscience format Example of Journal of Molecular Neuroscience format Example of Journal of Molecular Neuroscience format Example of Journal of Molecular Neuroscience format Example of Journal of Molecular Neuroscience format Example of Journal of Molecular Neuroscience format Example of Journal of Molecular Neuroscience format Example of Journal of Molecular Neuroscience format Example of Journal of Molecular Neuroscience format Example of Journal of Molecular Neuroscience format Example of Journal of Molecular Neuroscience format Example of Journal of Molecular Neuroscience format Example of Journal of Molecular Neuroscience format Example of Journal of Molecular Neuroscience format
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Example of Journal of Molecular Neuroscience format Example of Journal of Molecular Neuroscience format Example of Journal of Molecular Neuroscience format Example of Journal of Molecular Neuroscience format Example of Journal of Molecular Neuroscience format Example of Journal of Molecular Neuroscience format Example of Journal of Molecular Neuroscience format Example of Journal of Molecular Neuroscience format Example of Journal of Molecular Neuroscience format Example of Journal of Molecular Neuroscience format Example of Journal of Molecular Neuroscience format Example of Journal of Molecular Neuroscience format Example of Journal of Molecular Neuroscience format Example of Journal of Molecular Neuroscience format Example of Journal of Molecular Neuroscience format Example of Journal of Molecular Neuroscience format Example of Journal of Molecular Neuroscience format Example of Journal of Molecular Neuroscience format
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open access Open Access

Journal of Molecular Neuroscience — Template for authors

Publisher: Springer
Categories Rank Trend in last 3 yrs
Cellular and Molecular Neuroscience #61 of 88 down down by 9 ranks
journal-quality-icon Journal quality:
Medium
calendar-icon Last 4 years overview: 718 Published Papers | 3308 Citations
indexed-in-icon Indexed in: Scopus
last-updated-icon Last updated: 11/07/2020
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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.

2.678

4% from 2018

Impact factor for Journal of Molecular Neuroscience from 2016 - 2019
Year Value
2019 2.678
2018 2.577
2017 2.454
2016 2.229
graph view Graph view
table view Table view

4.6

2% from 2019

CiteRatio for Journal of Molecular Neuroscience from 2016 - 2020
Year Value
2020 4.6
2019 4.5
2018 4.6
2017 4.8
2016 4.6
graph view Graph view
table view Table view

insights Insights

  • Impact factor of this journal has increased by 4% in last year.
  • This journal’s impact factor is in the top 10 percentile category.

insights Insights

  • CiteRatio of this journal has increased by 2% 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.

0.936

9% from 2019

SJR for Journal of Molecular Neuroscience from 2016 - 2020
Year Value
2020 0.936
2019 0.861
2018 0.933
2017 0.974
2016 0.951
graph view Graph view
table view Table view

0.755

7% from 2019

SNIP for Journal of Molecular Neuroscience from 2016 - 2020
Year Value
2020 0.755
2019 0.704
2018 0.693
2017 0.672
2016 0.647
graph view Graph view
table view Table view

insights Insights

  • SJR of this journal has increased by 9% in last years.
  • This journal’s SJR is in the top 10 percentile category.

insights Insights

  • SNIP of this journal has increased by 7% in last years.
  • This journal’s SNIP is in the top 10 percentile category.

Journal of Molecular Neuroscience

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Springer

Journal of Molecular Neuroscience

The Journal of Molecular Neuroscience is committed to the rapid publication of original findings that increase our understanding of the molecular structure, function, and development of the nervous system. The criteria for acceptance of manuscripts will be scientific excellenc...... Read More

Medicine

i
Last updated on
11 Jul 2020
i
ISSN
0895-8696
i
Impact Factor
High - 2.229
i
Acceptance Rate
Not provided
i
Frequency
Not provided
i
Open Access
Yes
i
Sherpa RoMEO Archiving Policy
Green faq
i
Endnote Style
Download Available
i
Bibliography Name
SPBASIC
i
Citation Type
Author Year
(Blonder et al, 1982)
i
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/S12031-007-0029-0
Diffusion Tensor Imaging (DTI)-based White Matter Mapping in Brain Research: A Review
Yaniv Assaf1, Ofer Pasternak1

Abstract:

Diffusion tensor imaging (DTI) has become one of the most popular MRI techniques in brain research, as well as in clinical practice. The number of brain studies with DTI is growing steadily and, over the last decade, has produced more than 700 publications. Diffusion tensor imaging enables visualization and characterization o... Diffusion tensor imaging (DTI) has become one of the most popular MRI techniques in brain research, as well as in clinical practice. The number of brain studies with DTI is growing steadily and, over the last decade, has produced more than 700 publications. Diffusion tensor imaging enables visualization and characterization of white matter fascicli in two and three dimensions. Since the introduction of this methodology in 1994, it has been used to study the white matter architecture and integrity of the normal and diseased brains (multiple sclerosis, stroke, aging, dementia, schizophrenia, etc.). Although it provided image contrast that was not available with routine MR techniques, unique information on white matter and 3D visualization of neuronal pathways, many questions were raised regarding the origin of the DTI signal. Diffusion tensor imaging is constantly validated, challenged, and developed in terms of acquisition scheme, image processing, analysis, and interpretation. While DTI offers a powerful tool to study and visualize white matter, it suffers from inherent artifacts and limitations. The partial volume effect and the inability of the model to cope with non-Gaussian diffusion are its two main drawbacks. Nevertheless, when combined with functional brain mapping, DTI provides an efficient tool for comprehensive, noninvasive, functional anatomy mapping of the human brain. This review summarizes the development of DTI in the last decade with respect to the specificity and utility of the technique in radiology and anatomy studies. read more read less
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1,541 Citations
Journal Article DOI: 10.1385/JMN:23:1-2:105
BACE1: the beta-secretase enzyme in Alzheimer's disease.

Abstract:

Data that have accumulated for well over a decade have implicated the beta-amyloid (Abeta) peptide as a central player in the pathogenesis of Alzheimer's disease (AD) Amyloid plaques, composed primarily of Abeta progressively form in the brains of AD patients, and mutations in three genes (amyloid precursor protein [APP] and ... Data that have accumulated for well over a decade have implicated the beta-amyloid (Abeta) peptide as a central player in the pathogenesis of Alzheimer's disease (AD) Amyloid plaques, composed primarily of Abeta progressively form in the brains of AD patients, and mutations in three genes (amyloid precursor protein [APP] and presenilin 1 and 2 [PS1 and PS2]) cause early-onset familial AD (FAD) by directly increasing production of the toxic, plaque-promoting Abeta42 peptide Given the strong association between Abeta and AD, it is likely that therapeutic strategies to lower the levels of Abeta in the brain should prove beneficial for the treatment of AD One such strategy could involve inhibiting the enzymes that generate Abeta Abeta is a product of catabolism of the large type-I membrane protein APP Two proteases, called beta- and gamma-secretase, endoproteolyze APP to liberate the Abeta peptide Recently, the molecules responsible for these proteolytic activities have been identified Several lines of evidence suggest that the PS1 and PS2 proteins are gamma-secretase, and the identity of beta-secretase has been shown to be the novel transmembrane aspartic protease, beta-site APP-cleaving enzyme 1 (BACE1; also called Asp2 and memapsin 2) BACE2, a protease homologous to BACE1, was also identified, and together the two enzymes define a new family of transmembrane aspartic proteases BACE1 exhibits all the functional properties of beta-secretase, and as the key enzyme that initiates the formation of Abeta, BACE1 is an attractive drug target for AD This review discusses the identification and initial characterization of BACE1 and BACE2, and summarizes recent studies of BACE1 knockout mice that have validated BACE1 as the authentic beta-secretase in vivo read more read less
390 Citations
Journal Article DOI: 10.1007/S12031-011-9496-4
Specific Role of Tight Junction Proteins Claudin-5, Occludin, and ZO-1 of the Blood–Brain Barrier in a Focal Cerebral Ischemic Insult
Haixia Jiao1, Zhenhua Wang1, Yunhui Liu1, Ping Wang1, Yixue Xue1

Abstract:

Blood–brain barrier (BBB) leakage plays a key role in cerebral ischemia–reperfusion injury. It is quite necessary to further explore the characteristic and mechanism of BBB leakage during stroke. We induced a focal cerebral ischemia model by transient middle cerebral artery occlusion in male rats for defining the time course ... Blood–brain barrier (BBB) leakage plays a key role in cerebral ischemia–reperfusion injury. It is quite necessary to further explore the characteristic and mechanism of BBB leakage during stroke. We induced a focal cerebral ischemia model by transient middle cerebral artery occlusion in male rats for defining the time course of BBB permeability within 120 h following reperfusion and evaluate the specific role of tight junction (TJ) associated proteins claudin-5, occludin, and ZO-1 as well as protein kinase C delta (PKCδ) pathway in BBB leakage induced by reperfusion injury. We verified a bimodal increase in the permeability of the BBB following focal ischemia by Evans blue assay. Two peaks of BBB permeability appeared at 3 h and 72 h of reperfusion after 2 h focal ischemia, respectively. The leak at the endothelial cell was represented at the level of transmission electron microscopy. TTC staining results showed increased infarct size with time after cerebral ischemia reperfusion. The mRNA and protein expression levels of these three TJ associated proteins were significantly decreased compared with the sham-operated group within 120 h of reperfusion, corresponding to the time-dependent change of the biphasic pattern in BBB leakage. The redistribution of claudin-5, occludin, and ZO-1 in ischemia brain microvascular endothelial cells was observed at the same time points. In addition, Western blot assay revealed PKCδ level was also significantly increased in a similar biphasic pattern to above results within 120 h after cerebral ischemia–reperfusion. This study demonstrates the timing of TJ associated proteins claudin-5, occludin, and ZO-1 in light of BBB permeability associated with cerebral ischemia reperfusion, and suggests PKCδ pathway may participate in TJ barrier open and BBB leakage during reperfusion injury in a time-dependent manner. read more read less
374 Citations
Journal Article DOI: 10.1385/JMN:17:1:45
AMP-activated protein kinase is highly expressed in neurons in the developing rat brain and promotes neuronal survival following glucose deprivation.
Carsten Culmsee1, Jennifer Monnig2, Bruce E. Kemp3, Mark P. Mattson2, Mark P. Mattson4, Mark P. Mattson1

Abstract:

Adenosine monophosphate-activated protein kinase (AMPK) is a member of metabolite-sensing kinase family that plays important roles in responses of muscle cells to metabolic stress. AMPK is a heterotrimer of a catalytic alpha subunit (alpha1 or alpha2), and beta (beta1 or beta2) and gamma (gamma1 or gamma2) subunits. Because t... Adenosine monophosphate-activated protein kinase (AMPK) is a member of metabolite-sensing kinase family that plays important roles in responses of muscle cells to metabolic stress. AMPK is a heterotrimer of a catalytic alpha subunit (alpha1 or alpha2), and beta (beta1 or beta2) and gamma (gamma1 or gamma2) subunits. Because the brain has a high metabolic rate and is sensitive to changes in the supply of glucose and oxygen, we investigated the expression of AMPK in rat embryonic and adult brain and its role in modifying neuronal survival under conditions of cellular stress. We report that catalytic (alpha1 and alpha2) and noncatalytic (beta2 and gamma1) subunits of AMPK are present at high levels in embryonic hippocampal neurons in vivo and in cell culture. In the adult rat brain, the catalytic subunits alpha1 and alpha2 are present in neurons throughout the brain. The AMPK-activating agent AICAR protected hippocampal neurons against death induced by glucose deprivation, chemical hypoxia, and exposure to glutamate and amyloid beta-peptide. Suppression of levels of the AMPK alpha1 and alpha2 subunits using antisense technology resulted in enhanced neuronal death following glucose deprivation, and abolished the neuroprotective effect of AICAR. These findings suggest that AMPK can protect neurons against metabolic and excitotoxic insults relevant to the pathogenesis of several different neurodegenerative conditions. read more read less
361 Citations
open accessOpen access Journal Article DOI: 10.1007/S12031-011-9589-0
Neuropathology of frontotemporal lobar degeneration-tau (FTLD-tau).
Dennis W. Dickson1, Naomi Kouri1, Melissa E. Murray1, Keith A. Josephs

Abstract:

A clinically and pathologically heterogeneous type of frontotemporal lobar degeneration has abnormal tau pathology in neurons and glia (FTLD-tau). Familial FTLD-tau is usually due to mutations in the tau gene (MAPT). Even FTLD-tau determined by MAPT mutations has clinical and pathologic heterogeneity. Tauopathies are subclass... A clinically and pathologically heterogeneous type of frontotemporal lobar degeneration has abnormal tau pathology in neurons and glia (FTLD-tau). Familial FTLD-tau is usually due to mutations in the tau gene (MAPT). Even FTLD-tau determined by MAPT mutations has clinical and pathologic heterogeneity. Tauopathies are subclassified according to the predominant species of tau that accumulates, with respect to alternative splicing of MAPT, with tau proteins containing three (3R) or four repeats (4R) of ~32 amino acids in the microtubule binding domain. In Pick's disease (PiD), 3R tau predominates, whereas 4R tau is characteristic of corticobasal degeneration (CBD) and progressive supranuclear palsy (PSP). Depending upon the specific mutation in MAPT, familial FTLD-tau can have 3R, 4R or a combination of 3R and 4R tau. PiD is the least common FTLD-tau characterized by neuronal Pick bodies in a stereotypic neuroanatomical distribution. PSP and CBD are more common than PiD and have extensive clinical and pathologic overlap, with no distinctive clinical syndrome or biomarker that permits their differentiation. Diagnosis rests upon postmortem examination of the brain and demonstration of globose tangles, oligodendroglial coiled bodies and tufted astrocytes in PSP or threads, pretangles and astrocytic plaques in CBD. The anatomical distribution of tau pathology determines the clinical presentation of PSP and CBD, as well as PiD. The basis for this selective cortical vulnerability in FTLD-tau is unknown. read more read less
354 Citations
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3. Can I cite my article in multiple styles in Journal of Molecular Neuroscience?

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 Journal of Molecular Neuroscience citation style.

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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 Journal of Molecular Neuroscience.

5. Can I use a manuscript in Journal of Molecular Neuroscience 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 Journal of Molecular Neuroscience that you can download at the end.

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SciSpace's Journal of Molecular Neuroscience 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.

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

12. Is Journal of Molecular Neuroscience'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 Journal of Molecular Neuroscience?

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 Journal of Molecular Neuroscience. 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 Journal of Molecular Neuroscience?

The 5 most common citation types in order of usage for Journal of Molecular Neuroscience 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 Journal of Molecular Neuroscience?

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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 to SciSpace. Then SciSpace would allow you to download your references in Journal of Molecular Neuroscience Endnote style according to Elsevier guidelines.

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