Example of Brain Pathology format
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Example of Brain Pathology format Example of Brain Pathology format Example of Brain Pathology format Example of Brain Pathology format Example of Brain Pathology format Example of Brain Pathology format Example of Brain Pathology format Example of Brain Pathology format Example of Brain Pathology format Example of Brain Pathology format Example of Brain Pathology format Example of Brain Pathology format Example of Brain Pathology format Example of Brain Pathology format Example of Brain Pathology format Example of Brain Pathology format Example of Brain Pathology format Example of Brain Pathology format Example of Brain Pathology format Example of Brain Pathology format Example of Brain Pathology format
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Example of Brain Pathology format Example of Brain Pathology format Example of Brain Pathology format Example of Brain Pathology format Example of Brain Pathology format Example of Brain Pathology format Example of Brain Pathology format Example of Brain Pathology format Example of Brain Pathology format Example of Brain Pathology format Example of Brain Pathology format Example of Brain Pathology format Example of Brain Pathology format Example of Brain Pathology format Example of Brain Pathology format Example of Brain Pathology format Example of Brain Pathology format Example of Brain Pathology format Example of Brain Pathology format Example of Brain Pathology format Example of Brain Pathology format
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open access Open Access
recommended Recommended

Brain Pathology — Template for authors

Publisher: Wiley
Categories Rank Trend in last 3 yrs
Pathology and Forensic Medicine #8 of 191 -
Neurology (clinical) #27 of 343 down down by 3 ranks
Neuroscience (all) #16 of 110 -
journal-quality-icon Journal quality:
High
calendar-icon Last 4 years overview: 315 Published Papers | 2926 Citations
indexed-in-icon Indexed in: Scopus
last-updated-icon Last updated: 24/06/2020
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Related Journals

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Quality:  
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CiteRatio: 23.3
SJR: 7.183
SNIP: 3.099

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.

5.568

10% from 2018

Impact factor for Brain Pathology from 2016 - 2019
Year Value
2019 5.568
2018 6.155
2017 6.187
2016 5.272
graph view Graph view
table view Table view

9.3

CiteRatio for Brain Pathology from 2016 - 2020
Year Value
2020 9.3
2019 9.3
2018 9.1
2017 9.7
2016 9.0
graph view Graph view
table view Table view

insights Insights

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

insights Insights

  • 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.

1.986

9% from 2019

SJR for Brain Pathology from 2016 - 2020
Year Value
2020 1.986
2019 1.827
2018 2.185
2017 2.265
2016 2.407
graph view Graph view
table view Table view

1.35

9% from 2019

SNIP for Brain Pathology from 2016 - 2020
Year Value
2020 1.35
2019 1.234
2018 1.35
2017 1.389
2016 1.194
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 9% in last years.
  • This journal’s SNIP is in the top 10 percentile category.

Brain Pathology

Guideline source: View

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Wiley

Brain Pathology

Brain Pathology is the journal of choice for biomedical scientists investigating diseases of the nervous system. The official journal of the International Society of Neuropathology, Brain Pathology is a peer-reviewed bimonthly publication that includes original research, revie...... Read More

Medicine

i
Last updated on
23 Jun 2020
i
ISSN
1015-6305
i
Impact Factor
High - 1.233
i
Open Access
Yes
i
Sherpa RoMEO Archiving Policy
Yellow faq
i
Plagiarism Check
Available via Turnitin
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Endnote Style
Download Available
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Bibliography Name
apa
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Citation Type
Numbered
[25]
i
Bibliography Example
Beenakker, C.W.J. (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: 10.1111/J.1750-3639.1993.TB00752.X
The new WHO classification of brain tumours.
Paul Kleihues1, Peter C. Burger2, Bernd W. Scheithauer3
01 Jul 1993 - Brain Pathology

Abstract:

The new edition of the World Health Organization (WHO) book on 'Histological Typing of Tumours of the Central Nervous System' reflects the progress in brain tumour classification which has been achieved since publication of the first edition in 1979. Several new tumour entities have been added, including the pleomorphic xanth... The new edition of the World Health Organization (WHO) book on 'Histological Typing of Tumours of the Central Nervous System' reflects the progress in brain tumour classification which has been achieved since publication of the first edition in 1979. Several new tumour entities have been added, including the pleomorphic xanthoastrocytoma, central neurocytoma, the infantile desmoplastic astrocytoma/ganglioglioma, and the dysembryoplastic neuroepithelial tumour. The list of histological variants has also been expanded. In line with recent morphological and molecular data on glioma progression, the glioblastoma is now grouped together with astrocytic tumours. The classification of childhood tumours has been largely retained, the diagnosis primitive neuroectodermal tumour (PNET) only being recommended as a generic term for cerebellar medulloblastomas and neoplasms that are histologically indistinguishable from medulloblastoma but located in the CNS at sites other than the cerebellum. The WHO grading scheme was revised and adapted to new entities but its use, as before, remains optional. read more read less

Topics:

Central neurocytoma (57%)57% related to the paper, Pleomorphic xanthoastrocytoma (55%)55% related to the paper, Ganglioglioma (54%)54% related to the paper, Astrocytoma (50%)50% related to the paper
1,532 Citations
open accessOpen access Journal Article DOI: 10.1111/J.1750-3639.2004.TB00049.X
Detection of Ectopic B-cell Follicles with Germinal Centers in the Meninges of Patients with Secondary Progressive Multiple Sclerosis
Barbara Serafini1, Barbara Rosicarelli1, Roberta Magliozzi1, Egidio Stigliano, Francesca Aloisi1
01 Apr 2004 - Brain Pathology

Abstract:

Multiple sclerosis (MS) is characterized by synthesis of oligoclonal immunoglobulins and the presence of B-cell clonal expansions in the central nervous system (CNS). Because ectopic lymphoid tissue generated at sites of chronic inflammation is thought to be important in sustaining immunopathological processes, we have invest... Multiple sclerosis (MS) is characterized by synthesis of oligoclonal immunoglobulins and the presence of B-cell clonal expansions in the central nervous system (CNS). Because ectopic lymphoid tissue generated at sites of chronic inflammation is thought to be important in sustaining immunopathological processes, we have investigated whether structures resembling lymphoid follicles could be identified in the CNS of MS patients. Sections from post-mortem MS brains and spinal cords were screened using immunohistochemistry for the presence of CD20+ B-cells, CD3+ T-cells, CD138+ plasma cells and CD21+, CD35+ follicular dendritic cells, and for the expression of lymphoid chemokines (CXCL 13, CCL21) and peripheral node addressin (PNAd). Lymphoid follicle-like structures containing B-cells, T-cells and plasma cells, and a network of follicular dendritic cells producing CXCL13 were observed in the cerebral meninges of 2 out of 3 patients with secondary progressive MS, but not in relapsing remitting and primary progressive MS. We also show that proliferating B-cells are present in intrameningeal follicles, a finding which is suggestive of germinal center formation. No follicle-like structures were detected in parenchymal lesions. The formation of ectopic lymphoid follicies in the meninges of patients with MS could represent a critical step in maintaining humoral autoimmunity and in disease exacerbation. read more read less

Topics:

Follicular dendritic cells (63%)63% related to the paper, Germinal center (58%)58% related to the paper, CXCL13 (54%)54% related to the paper, B cell (53%)53% related to the paper, Lymphatic system (52%)52% related to the paper
1,063 Citations
open accessOpen access Journal Article DOI: 10.1111/J.1750-3639.2007.00064.X
The immunopathology of multiple sclerosis: An overview
Hans Lassmann1, Wolfgang Brück2, Claudia F. Lucchinetti3
01 Apr 2007 - Brain Pathology

Abstract:

Multiple sclerosis (MS) is traditionally seen as an inflammatory demyelinating disease, characterized by the formation of focal demyelinated plaques in the white matter of the central nervous system. In this review we describe recent evidence that the spectrum of MS pathology is much broader. This includes demyelination in th... Multiple sclerosis (MS) is traditionally seen as an inflammatory demyelinating disease, characterized by the formation of focal demyelinated plaques in the white matter of the central nervous system. In this review we describe recent evidence that the spectrum of MS pathology is much broader. This includes demyelination in the cortex and deep gray matter nuclei, as well as diffuse injury of the normal-appearing white matter. The mechanisms responsible for the formation of focal lesions in different patients and in different stages of the disease as well as those involved in the induction of diffuse brain damage are complex and heterogeneous. This heterogeneity is reflected by different clinical manifestations of the disease, such as relapsing or progressive MS, and also explains at least in part the relation of MS to other inflammatory demyelinating diseases. read more read less

Topics:

Multiple sclerosis (57%)57% related to the paper, White matter (51%)51% related to the paper
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1,055 Citations
open accessOpen access Journal Article DOI: 10.1111/J.1750-3639.2001.TB00385.X
The Neurotoxicant, Cuprizone, as a Model to Study Demyelination and Remyelination in the Central Nervous System
Glenn K. Matsushima1, Pierre Morell1
05 Apr 2006 - Brain Pathology

Abstract:

Myelin of the adult CNS is vulnerable to a variety of metabolic, toxic, and autoimmune insults. That remyelination can ensue, following demyelinating insult, has been well demonstrated. Details of the process of remyelination are, however difficult to ascertain since in most experimental models of demyelination/remyelination ... Myelin of the adult CNS is vulnerable to a variety of metabolic, toxic, and autoimmune insults. That remyelination can ensue, following demyelinating insult, has been well demonstrated. Details of the process of remyelination are, however difficult to ascertain since in most experimental models of demyelination/remyelination the severity, localization of lesion site, or time course of the pathophysiology is variable from animal to animal. In contrast, an experimental model in which massive demyelination can be reproducibly induced in large areas of mouse brain is exposure to the copper chelator, cuprizone, in the diet. We review work from several laboratories over the past 3 decades, with emphasis on our own recent studies, which suggest an overall picture of cellular events involved in demyelination/remyelination. When 8 week old C57BL/6 mice are fed 0.2% cuprizone in the diet, mature olidgodendroglia are specifically insulted (cannot fulfill the metabolic demand of support of vast amounts of myelin) and go through apoptosis.This is closely followed by recruitment of microglia and phagoctytosis of myelin. Studies of myelin gene expression, coordinated with morphological studies, indicate that even in the face of continued metabolic challenge, oligodendroglial progenitor cells proliferate and invade demyelinated areas. If the cuprizone challenge is terminated, an almost complete remyelination takes place in a matter of weeks. Communication between different cell types by soluble factors may be inferred. This material is presented in the context of a model compatible with present data—and which can be tested more rigorously with the cuprizone model. The reproducibility of the model indicates that it may allow for testing of manipulations (e.g. available knockouts or transgenics on the common genetic background, or pharmacological treatments) which may accelerate or repress the process of demyelination and or remyelination. read more read less

Topics:

Remyelination (66%)66% related to the paper, Myelin (52%)52% related to the paper
870 Citations
Journal Article DOI: 10.1111/J.1750-3639.1994.TB00838.X
GFAP and Astrogliosis
Lawrence F. Eng1, Roopa S. Ghirnikar2
01 Jul 1994 - Brain Pathology

Abstract:

One of the most remarkable characteristics of astrocytes is their vigorous response to diverse neurologic insults, a feature that is well conserved across a variety of different species. The astroglial response occurs rapidly and can be detected within one hour of a focal mechanical trauma (Mucke et al., 1991). Prominent reac... One of the most remarkable characteristics of astrocytes is their vigorous response to diverse neurologic insults, a feature that is well conserved across a variety of different species. The astroglial response occurs rapidly and can be detected within one hour of a focal mechanical trauma (Mucke et al., 1991). Prominent reactive astrogliosis is seen; in AIDS dementia; a variety of other viral infections; prion associated spongiform encephalopathies; inflammatory demyelinating diseases; acute traumatic brain injury; neurodegenerative diseases such as Alzheimer's disease. The prominence of astroglial reactions in various diseases, the rapidity of the astroglial response and the evolutionary conservation of reactive astrogliosis indicate that reactive astrocytes fulfill important functions of the central nervous system (CNS). Yet, the exact role reactive astrocytes play in the injured CNS has so far remained elusive. This chapter summaries the various experimental models and diseases that exhibit astrogliosis and increase in glial fibrillary acidic protein (GFAP). Recent in vitro studies to inhibit GFAP synthesis are also presented. read more read less

Topics:

Astrogliosis (67%)67% related to the paper, Glial fibrillary acidic protein (54%)54% related to the paper
816 Citations
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Brain Pathology format uses apa citation style.

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Frequently asked questions

1. Can I write Brain Pathology in LaTeX?

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

2. Do you follow the Brain Pathology guidelines?

Yes, the template is compliant with the Brain Pathology 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 Brain Pathology?

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 Brain Pathology citation style.

4. Can I use the Brain Pathology 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 Brain Pathology.

5. Can I use a manuscript in Brain Pathology 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 Brain Pathology that you can download at the end.

6. How long does it usually take you to format my papers in Brain Pathology?

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

7. Where can I find the template for the Brain Pathology?

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 Brain Pathology'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 Brain Pathology'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. Brain Pathology an online tool or is there a desktop version?

SciSpace's Brain Pathology 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 Brain Pathology?

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 Brain Pathology?”

11. What is the output that I would get after using Brain Pathology?

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

12. Is Brain Pathology'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 Brain Pathology?

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 Brain Pathology. 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 Brain Pathology?

The 5 most common citation types in order of usage for Brain Pathology 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 Brain Pathology?

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

16. Can I download Brain Pathology 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 Brain Pathology Endnote style according to Elsevier guidelines.

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I spent hours with MS word for reformatting. It was frustrating - plain and simple. With SciSpace, I can draft my manuscripts and once it is finished I can just submit. In case, I have to submit to another journal it is really just a button click instead of an afternoon of reformatting.

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