Example of Molecular Neurodegeneration format
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Example of Molecular Neurodegeneration format Example of Molecular Neurodegeneration format Example of Molecular Neurodegeneration format Example of Molecular Neurodegeneration format Example of Molecular Neurodegeneration format Example of Molecular Neurodegeneration format Example of Molecular Neurodegeneration format Example of Molecular Neurodegeneration format Example of Molecular Neurodegeneration format Example of Molecular Neurodegeneration format Example of Molecular Neurodegeneration format Example of Molecular Neurodegeneration format Example of Molecular Neurodegeneration format Example of Molecular Neurodegeneration format Example of Molecular Neurodegeneration format Example of Molecular Neurodegeneration format Example of Molecular Neurodegeneration format Example of Molecular Neurodegeneration format
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Example of Molecular Neurodegeneration format Example of Molecular Neurodegeneration format Example of Molecular Neurodegeneration format Example of Molecular Neurodegeneration format Example of Molecular Neurodegeneration format Example of Molecular Neurodegeneration format Example of Molecular Neurodegeneration format Example of Molecular Neurodegeneration format Example of Molecular Neurodegeneration format Example of Molecular Neurodegeneration format Example of Molecular Neurodegeneration format Example of Molecular Neurodegeneration format Example of Molecular Neurodegeneration format Example of Molecular Neurodegeneration format Example of Molecular Neurodegeneration format Example of Molecular Neurodegeneration format Example of Molecular Neurodegeneration format Example of Molecular Neurodegeneration format
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recommended Recommended

Molecular Neurodegeneration — Template for authors

Publisher: Springer
Categories Rank Trend in last 3 yrs
Neurology (clinical) #7 of 343 up up by 11 ranks
Molecular Biology #17 of 382 up up by 27 ranks
Cellular and Molecular Neuroscience #5 of 88 up up by 4 ranks
journal-quality-icon Journal quality:
High
calendar-icon Last 4 years overview: 266 Published Papers | 5070 Citations
indexed-in-icon Indexed in: Scopus
last-updated-icon Last updated: 03/07/2020
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Related Journals

open access Open Access
recommended Recommended

PLOS

Quality:  
High
CiteRatio: 7.3
SJR: 2.628
SNIP: 1.713
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Nature

Quality:  
High
CiteRatio: 29.5
SJR: 7.271
SNIP: 5.939
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Frontiers Media

Quality:  
High
CiteRatio: 8.4
SJR: 1.989
SNIP: 1.224
open access Open Access
recommended Recommended

Springer

Quality:  
High
CiteRatio: 8.2
SJR: 3.131
SNIP: 1.18

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.

9.599

16% from 2018

Impact factor for Molecular Neurodegeneration from 2016 - 2019
Year Value
2019 9.599
2018 8.274
2017 6.426
2016 6.78
graph view Graph view
table view Table view

19.1

27% from 2019

CiteRatio for Molecular Neurodegeneration from 2016 - 2020
Year Value
2020 19.1
2019 15.0
2018 11.3
2017 10.3
2016 10.5
graph view Graph view
table view Table view

insights Insights

  • Impact factor of this journal has increased by 16% in last year.
  • This journal’s impact factor is in the top 10 percentile category.

insights Insights

  • CiteRatio of this journal has increased by 27% 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.

5.565

38% from 2019

SJR for Molecular Neurodegeneration from 2016 - 2020
Year Value
2020 5.565
2019 4.04
2018 3.988
2017 3.418
2016 3.684
graph view Graph view
table view Table view

2.172

30% from 2019

SNIP for Molecular Neurodegeneration from 2016 - 2020
Year Value
2020 2.172
2019 1.671
2018 1.487
2017 1.313
2016 1.28
graph view Graph view
table view Table view

insights Insights

  • SJR of this journal has increased by 38% in last years.
  • This journal’s SJR is in the top 10 percentile category.

insights Insights

  • SNIP of this journal has increased by 30% in last years.
  • This journal’s SNIP is in the top 10 percentile category.

Molecular Neurodegeneration

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Springer

Molecular Neurodegeneration

Approved by publishing and review experts on SciSpace, this template is built as per for Molecular Neurodegeneration formatting guidelines as mentioned in Springer author instructions. The current version was created on and has been used by 593 authors to write and format their manuscripts to this journal.

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Last updated on
02 Jul 2020
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ISSN
1606-8610
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Open Access
Yes
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Sherpa RoMEO Archiving Policy
White faq
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Plagiarism Check
Available via Turnitin
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Endnote Style
Download Available
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Citation Type
Numbered
[25]
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Bibliography Example
Blonder, G.E., Tinkham, M., Klapwijk, T.M.: Transition from metallic to tunneling regimes in superconducting microconstrictions: Excess current, charge imbalance, and supercurrent conversion. Phys. Rev. B 25(7), 4515–4532 (1982)

Top papers written in this journal

open accessOpen access Journal Article DOI: 10.1186/S13024-019-0333-5
The neuropathological diagnosis of Alzheimer's disease.
Michael DeTure1, Dennis W. Dickson1

Abstract:

Alzheimer’s disease is a progressive neurodegenerative disease most often associated with memory deficits and cognitive decline, although less common clinical presentations are increasingly recognized. The cardinal pathological features of the disease have been known for more than one hundred years, and today the presence of ... Alzheimer’s disease is a progressive neurodegenerative disease most often associated with memory deficits and cognitive decline, although less common clinical presentations are increasingly recognized. The cardinal pathological features of the disease have been known for more than one hundred years, and today the presence of these amyloid plaques and neurofibrillary tangles are still required for a pathological diagnosis. Alzheimer’s disease is the most common cause of dementia globally. There remain no effective treatment options for the great majority of patients, and the primary causes of the disease are unknown except in a small number of familial cases driven by genetic mutations. Confounding efforts to develop effective diagnostic tools and disease-modifying therapies is the realization that Alzheimer’s disease is a mixed proteinopathy (amyloid and tau) frequently associated with other age-related processes such as cerebrovascular disease and Lewy body disease. Defining the relationships between and interdependence of various co-pathologies remains an active area of investigation. This review outlines etiologically-linked pathologic features of Alzheimer’s disease, as well as those that are inevitable findings of uncertain significance, such as granulovacuolar degeneration and Hirano bodies. Other disease processes that are frequent, but not inevitable, are also discussed, including pathologic processes that can clinically mimic Alzheimer’s disease. These include cerebrovascular disease, Lewy body disease, TDP-43 proteinopathies and argyrophilic grain disease. The purpose of this review is to provide an overview of Alzheimer’s disease pathology, its defining pathologic substrates and the related pathologies that can affect diagnosis and treatment. read more read less

Topics:

Dementia (64%)64% related to the paper, Neuropathology (54%)54% related to the paper, Disease (53%)53% related to the paper, Cognitive decline (51%)51% related to the paper
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1,228 Citations
open accessOpen access Journal Article DOI: 10.1186/1750-1326-6-85
Adult hippocampal neurogenesis and its role in Alzheimer's disease
Yangling Mu1, Fred H. Gage1

Abstract:

The hippocampus, a brain area critical for learning and memory, is especially vulnerable to damage at early stages of Alzheimer's disease (AD). Emerging evidence has indicated that altered neurogenesis in the adult hippocampus represents an early critical event in the course of AD. Although causal links have not been establis... The hippocampus, a brain area critical for learning and memory, is especially vulnerable to damage at early stages of Alzheimer's disease (AD). Emerging evidence has indicated that altered neurogenesis in the adult hippocampus represents an early critical event in the course of AD. Although causal links have not been established, a variety of key molecules involved in AD pathogenesis have been shown to impact new neuron generation, either positively or negatively. From a functional point of view, hippocampal neurogenesis plays an important role in structural plasticity and network maintenance. Therefore, dysfunctional neurogenesis resulting from early subtle disease manifestations may in turn exacerbate neuronal vulnerability to AD and contribute to memory impairment, whereas enhanced neurogenesis may be a compensatory response and represent an endogenous brain repair mechanism. Here we review recent findings on alterations of neurogenesis associated with pathogenesis of AD, and we discuss the potential of neurogenesis-based diagnostics and therapeutic strategies for AD. read more read less

Topics:

Neurogenesis (63%)63% related to the paper
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800 Citations
open accessOpen access Journal Article DOI: 10.1186/1750-1326-2-18
Fibril specific, conformation dependent antibodies recognize a generic epitope common to amyloid fibrils and fibrillar oligomers that is absent in prefibrillar oligomers

Abstract:

Amyloid-related degenerative diseases are associated with the accumulation of misfolded proteins as amyloid fibrils in tissue. In Alzheimer disease (AD), amyloid accumulates in several distinct types of insoluble plaque deposits, intracellular Aβ and as soluble oligomers and the relationships between these deposits and their ... Amyloid-related degenerative diseases are associated with the accumulation of misfolded proteins as amyloid fibrils in tissue. In Alzheimer disease (AD), amyloid accumulates in several distinct types of insoluble plaque deposits, intracellular Aβ and as soluble oligomers and the relationships between these deposits and their pathological significance remains unclear. Conformation dependent antibodies have been reported that specifically recognize distinct assembly states of amyloids, including prefibrillar oligomers and fibrils. We immunized rabbits with a morphologically homogeneous population of Aβ42 fibrils. The resulting immune serum (OC) specifically recognizes fibrils, but not random coil monomer or prefibrillar oligomers, indicating fibrils display a distinct conformation dependent epitope that is absent in prefibrillar oligomers. The fibril epitope is also displayed by fibrils of other types of amyloids, indicating that the epitope is a generic feature of the polypeptide backbone. The fibril specific antibody also recognizes 100,000 × G soluble fibrillar oligomers ranging in size from dimer to greater than 250 kDa on western blots. The fibrillar oligomers recognized by OC are immunologically distinct from prefibrillar oligomers recognized by A11, even though their sizes overlap broadly, indicating that size is not a reliable indicator of oligomer conformation. The immune response to prefibrillar oligomers and fibrils is not sequence specific and antisera of the same specificity are produced in response to immunization with islet amyloid polypeptide prefibrillar oligomer mimics and fibrils. The fibril specific antibodies stain all types of amyloid deposits in human AD brain. Diffuse amyloid deposits stain intensely with anti-fibril antibody although they are thioflavin S negative, suggesting that they are indeed fibrillar in conformation. OC also stains islet amyloid deposits in transgenic mouse models of type II diabetes, demonstrating its generic specificity for amyloid fibrils. Since the fibril specific antibodies are conformation dependent, sequence-independent, and recognize epitopes that are distinct from those present in prefibrillar oligomers, they may have broad utility for detecting and characterizing the accumulation of amyloid fibrils and fibrillar type oligomers in degenerative diseases. read more read less

Topics:

Amyloid (60%)60% related to the paper, Fibril (53%)53% related to the paper, Population (50%)50% related to the paper
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720 Citations
open accessOpen access Journal Article DOI: 10.1186/1750-1326-7-42
Exosomal cell-to-cell transmission of alpha synuclein oligomers

Abstract:

Aggregation of alpha-synuclein (αsyn) and resulting cytotoxicity is a hallmark of sporadic and familial Parkinson’s disease (PD) as well as dementia with Lewy bodies, with recent evidence implicating oligomeric and pre-fibrillar forms of αsyn as the pathogenic species. Recent in vitro studies support the idea of transcellular... Aggregation of alpha-synuclein (αsyn) and resulting cytotoxicity is a hallmark of sporadic and familial Parkinson’s disease (PD) as well as dementia with Lewy bodies, with recent evidence implicating oligomeric and pre-fibrillar forms of αsyn as the pathogenic species. Recent in vitro studies support the idea of transcellular spread of extracellular, secreted αsyn across membranes. The aim of this study is to characterize the transcellular spread of αsyn oligomers and determine their extracellular location. Using a novel protein fragment complementation assay where αsyn is fused to non-bioluminescent amino-or carboxy-terminus fragments of humanized Gaussia Luciferase we demonstrate here that αsyn oligomers can be found in at least two extracellular fractions: either associated with exosomes or free. Exosome-associated αsyn oligomers are more likely to be taken up by recipient cells and can induce more toxicity compared to free αsyn oligomers. Specifically, we determine that αsyn oligomers are present on both the outside as well as inside of exosomes. Notably, the pathway of secretion of αsyn oligomers is strongly influenced by autophagic activity. Our data suggest that αsyn may be secreted via different secretory pathways. We hypothesize that exosome-mediated release of αsyn oligomers is a mechanism whereby cells clear toxic αsyn oligomers when autophagic mechanisms fail to be sufficient. Preventing the early events in αsyn exosomal release and uptake by inducing autophagy may be a novel approach to halt disease spreading in PD and other synucleinopathies. read more read less
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711 Citations
open accessOpen access Journal Article DOI: 10.1186/1750-1326-4-47
Does neuroinflammation fan the flame in neurodegenerative diseases
Tamy C. Frank-Cannon1, Laura Taylor Alto2, Fiona E. Mcalpine3, Malú G. Tansey4

Abstract:

While peripheral immune access to the central nervous system (CNS) is restricted and tightly controlled, the CNS is capable of dynamic immune and inflammatory responses to a variety of insults. Infections, trauma, stroke, toxins and other stimuli are capable of producing an immediate and short lived activation of the innate i... While peripheral immune access to the central nervous system (CNS) is restricted and tightly controlled, the CNS is capable of dynamic immune and inflammatory responses to a variety of insults. Infections, trauma, stroke, toxins and other stimuli are capable of producing an immediate and short lived activation of the innate immune system within the CNS. This acute neuroinflammatory response includes activation of the resident immune cells (microglia) resulting in a phagocytic phenotype and the release of inflammatory mediators such as cytokines and chemokines. While an acute insult may trigger oxidative and nitrosative stress, it is typically short-lived and unlikely to be detrimental to long-term neuronal survival. In contrast, chronic neuroinflammation is a long-standing and often self-perpetuating neuroinflammatory response that persists long after an initial injury or insult. Chronic neuroinflammation includes not only long-standing activation of microglia and subsequent sustained release of inflammatory mediators, but also the resulting increased oxidative and nitrosative stress. The sustained release of inflammatory mediators works to perpetuate the inflammatory cycle, activating additional microglia, promoting their proliferation, and resulting in further release of inflammatory factors. Neurodegenerative CNS disorders, including multiple sclerosis (MS), Alzheimer's disease (AD), Parkinson's disease (PD), Huntington's disease (HD), amyotrophic lateral sclerosis (ALS), tauopathies, and age-related macular degeneration (ARMD), are associated with chronic neuroinflammation and elevated levels of several cytokines. Here we review the hallmarks of acute and chronic inflammatory responses in the CNS, the reasons why microglial activation represents a convergence point for diverse stimuli that may promote or compromise neuronal survival, and the epidemiologic, pharmacologic and genetic evidence implicating neuroinflammation in the pathophysiology of several neurodegenerative diseases. read more read less

Topics:

Neuroinflammation (61%)61% related to the paper, Neuroprotection (61%)61% related to the paper, Microglia (52%)52% related to the paper, Innate immune system (51%)51% related to the paper
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673 Citations
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Frequently asked questions

1. Can I write Molecular Neurodegeneration 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 Neurodegeneration guidelines and auto format it.

2. Do you follow the Molecular Neurodegeneration guidelines?

Yes, the template is compliant with the Molecular Neurodegeneration 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 Neurodegeneration?

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 Neurodegeneration citation style.

4. Can I use the Molecular Neurodegeneration 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 Neurodegeneration.

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

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

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 Neurodegeneration.

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

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 Neurodegeneration'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 Neurodegeneration'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 Neurodegeneration an online tool or is there a desktop version?

SciSpace's Molecular Neurodegeneration 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 Neurodegeneration?

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 Neurodegeneration?”

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

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

12. Is Molecular Neurodegeneration'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 Neurodegeneration?

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 Neurodegeneration. 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 Neurodegeneration?

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

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 Neurodegeneration's guidelines and download the same in Word, PDF and LaTeX formats? Give us a try!.

16. Can I download Molecular Neurodegeneration 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 Neurodegeneration Endnote style according to Elsevier guidelines.

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