Example of Metabolic Brain Disease format
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Example of Metabolic Brain Disease format Example of Metabolic Brain Disease format Example of Metabolic Brain Disease format Example of Metabolic Brain Disease format Example of Metabolic Brain Disease format Example of Metabolic Brain Disease format Example of Metabolic Brain Disease format Example of Metabolic Brain Disease format Example of Metabolic Brain Disease format Example of Metabolic Brain Disease format Example of Metabolic Brain Disease format Example of Metabolic Brain Disease format Example of Metabolic Brain Disease format Example of Metabolic Brain Disease format Example of Metabolic Brain Disease format Example of Metabolic Brain Disease format Example of Metabolic Brain Disease format Example of Metabolic Brain Disease format
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Example of Metabolic Brain Disease format Example of Metabolic Brain Disease format Example of Metabolic Brain Disease format Example of Metabolic Brain Disease format Example of Metabolic Brain Disease format Example of Metabolic Brain Disease format Example of Metabolic Brain Disease format Example of Metabolic Brain Disease format Example of Metabolic Brain Disease format Example of Metabolic Brain Disease format Example of Metabolic Brain Disease format Example of Metabolic Brain Disease format Example of Metabolic Brain Disease format Example of Metabolic Brain Disease format Example of Metabolic Brain Disease format Example of Metabolic Brain Disease format Example of Metabolic Brain Disease format Example of Metabolic Brain Disease format
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open access Open Access

Metabolic Brain Disease — Template for authors

Publisher: Springer
Categories Rank Trend in last 3 yrs
Neurology (clinical) #79 of 343 up up by 46 ranks
Biochemistry #141 of 415 up up by 63 ranks
Cellular and Molecular Neuroscience #42 of 88 up up by 23 ranks
journal-quality-icon Journal quality:
High
calendar-icon Last 4 years overview: 695 Published Papers | 3995 Citations
indexed-in-icon Indexed in: Scopus
last-updated-icon Last updated: 24/06/2020
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Related Journals

open access Open Access
recommended Recommended

Nature

Quality:  
High
CiteRatio: 29.5
SJR: 7.271
SNIP: 5.939
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Springer

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CiteRatio: 8.2
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CiteRatio: 23.3
SJR: 7.183
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open access Open Access

Springer

Quality:  
High
CiteRatio: 6.0
SJR: 1.239
SNIP: 1.096

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.

2.726

13% from 2018

Impact factor for Metabolic Brain Disease from 2016 - 2019
Year Value
2019 2.726
2018 2.411
2017 2.441
2016 2.297
graph view Graph view
table view Table view

5.7

27% from 2019

CiteRatio for Metabolic Brain Disease from 2016 - 2020
Year Value
2020 5.7
2019 4.5
2018 4.0
2017 4.0
2016 4.2
graph view Graph view
table view Table view

insights Insights

  • Impact factor of this journal has increased by 13% 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.

0.851

10% from 2019

SJR for Metabolic Brain Disease from 2016 - 2020
Year Value
2020 0.851
2019 0.775
2018 0.795
2017 0.909
2016 0.9
graph view Graph view
table view Table view

0.946

11% from 2019

SNIP for Metabolic Brain Disease from 2016 - 2020
Year Value
2020 0.946
2019 0.856
2018 0.778
2017 0.798
2016 0.813
graph view Graph view
table view Table view

insights Insights

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

insights Insights

  • SNIP of this journal has increased by 11% in last years.
  • This journal’s SNIP is in the top 10 percentile category.

Metabolic Brain Disease

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Springer

Metabolic Brain Disease

Metabolic Brain Disease serves as a forum for the publication of outstanding basic and clinical papers on all metabolic brain disease, including both human and animal studies. The journal publishes papers on the fundamental pathogenesis of these disorders and on related experi...... Read More

Clinical Neurology

Biochemistry

Cellular and Molecular Neuroscience

Medicine

i
Last updated on
23 Jun 2020
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ISSN
0885-7490
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Impact Factor
Medium - 0.822
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)
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/S11011-008-9118-1
The inflammatory & neurodegenerative (I&ND) hypothesis of depression: leads for future research and new drug developments in depression
01 Mar 2009 - Metabolic Brain Disease

Abstract:

Despite extensive research, the current theories on serotonergic dysfunctions and cortisol hypersecretion do not provide sufficient explanations for the nature of depression. Rational treatments aimed at causal factors of depression are not available yet. With the currently available antidepressant drugs, which mainly target ... Despite extensive research, the current theories on serotonergic dysfunctions and cortisol hypersecretion do not provide sufficient explanations for the nature of depression. Rational treatments aimed at causal factors of depression are not available yet. With the currently available antidepressant drugs, which mainly target serotonin, less than two thirds of depressed patients achieve remission. There is now evidence that inflammatory and neurodegenerative (IN established and novel animal and ex vivo-in vitro models for depression, such as new transgenic mouse models and endophenotype-based animal models, specific cell lines, in vivo and ex vivo electroporation, and organotypic brain slice culture models. This screening will allow to: 1) discover new IN and elucidate the underlying molecular IN and 2) identify new therapeutic targets in the IN develop new anti-IN select existing anti-IN and predict therapeutic response by genetic I&ND profiles. read more read less
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794 Citations
Journal Article DOI: 10.1023/B:MEBR.0000043966.46964.E6
Pathophysiology of stroke: lessons from animal models
Philipp Mergenthaler1, Ulrich Dirnagl1, Andreas Meisel1
01 Dec 2004 - Metabolic Brain Disease

Abstract:

The current pathophysiological understanding of stroke is substantially based on experimental studies. Brain injury after cerebral ischemia develops from a complex signaling cascade that evolves in an at least partially unraveled spatiotemporal pattern. Early excitotoxicity can lead to fast necrotic cell death, which produces... The current pathophysiological understanding of stroke is substantially based on experimental studies. Brain injury after cerebral ischemia develops from a complex signaling cascade that evolves in an at least partially unraveled spatiotemporal pattern. Early excitotoxicity can lead to fast necrotic cell death, which produces the core of the infarction. The ischemic penumbra that surrounds the infarct core suffers milder insults. In this area, both mild excitotoxic and inflammatory mechanisms lead to delayed cell death, which shows biochemical characteristics of apoptosis. While brain cells are challenged by these deleterious mechanisms, they activate innate protective programs of the brain, which can be studied by means of experimentally inducing ischemic tolerance (i.e., ischemic preconditioning). Importantly, cerebral ischemia not only affects the brain parenchyma, but also impacts extracranial systems. For example, stroke induces a dramatic immunosuppression via an overactivation of the sympathetic nervous system. As a result, severe bacterial infections such as pneumonia occur. Complex signaling cascades not only decide about cell survival, but also about the neurological deficit and the mortality after stroke. These mechanisms of damage and endogenous protection present distinct molecular targets that are the rational basis for the development of neuroprotective drugs. read more read less

Topics:

Penumbra (57%)57% related to the paper, Stroke (56%)56% related to the paper, Ischemia (54%)54% related to the paper, Excitotoxicity (53%)53% related to the paper
349 Citations
Journal Article DOI: 10.1007/BF02676357
Fundamental neuroscience: Duane E. Hanes Churchil Livingston, New York, 1997
01 Mar 1997 - Metabolic Brain Disease

Abstract:

Rather than enjoying a good book similar to a cup of coffee in the afternoon, instead they juggled considering some harmful virus inside their computer. fundamental neuroscience is manageable in our digital library an online permission to it is set as public in view of that you can download it instantly. Our digital library s... Rather than enjoying a good book similar to a cup of coffee in the afternoon, instead they juggled considering some harmful virus inside their computer. fundamental neuroscience is manageable in our digital library an online permission to it is set as public in view of that you can download it instantly. Our digital library saves in complex countries, allowing you to get the most less latency times to download any of our books once this one. Merely said, the fundamental neuroscience is universally compatible in the manner of any devices to read. read more read less
View PDF
337 Citations
Journal Article DOI: 10.1023/B:MEBR.0000027412.19664.B3
Maternal separation in rats leads to anxiety-like behavior and a blunted ACTH response and altered neurotransmitter levels in response to a subsequent stressor.
Willie M. U. Daniels1, Charmaine Y. Pietersen1, Machteld E. Carstens1, Dan J. Stein1
01 Jun 2004 - Metabolic Brain Disease

Abstract:

Adverse early life experiences can have a negative impact on behavior later in life We subjected rat pups to maternal separation and determined the effects thereof on adult behavior We removed rat pups from their mothers for 3 h daily from postnatal days 2 to 14 While controls were reared normally on day 60, the behaviors of ... Adverse early life experiences can have a negative impact on behavior later in life We subjected rat pups to maternal separation and determined the effects thereof on adult behavior We removed rat pups from their mothers for 3 h daily from postnatal days 2 to 14 While controls were reared normally on day 60, the behaviors of the rats were tested using the elevated plus-maze Some rats were subsequently subjected to restraint stress for a 10-min period Trunk blood was collected for basal, as well as 15- and 60-min postrestraint stress ACTH determinations Neurotransmitter levels (noradrenaline (NA), serotonin (5HT), and their metabolites, MHPG and 5HIAA, respectively) were also determined at basal, immediately and 15-min post-restraint stress in the hypothalamus, hippocampus, and frontal cortex in another group of animals The amount of entries into the arms of the elevated plus-maze was significantly reduced in the separated animals, indicating decreased locomotion They spent significantly more time in the closed arms of the maze A significant increase in defecation frequency was noted These observations suggested anxious behavior Basal ACTH levels were significantly higher in separated animals At 15-min post-restraint stress, the ACTH levels were significantly lower than controls, indicating a blunted stress response A decrease in noradrenaline was noted first in limbic regions and an increase in 5HIAA levels was found in the frontal cortex and hippocampus We conclude that maternal separation induced abnormal behaviors and stress responses that were associated with altered neurotransmitter levels read more read less

Topics:

Adrenocorticotropic hormone (53%)53% related to the paper, Elevated plus maze (52%)52% related to the paper
313 Citations
Journal Article DOI: 10.1023/A:1021989230535
Pathophysiology of hepatic encephalopathy: a new look at ammonia.
Roger F. Butterworth1
01 Dec 2002 - Metabolic Brain Disease

Abstract:

Results of neuropathologic, spectroscopic, and neurochemical studies continue to confirm a major role for ammonia in the pathogenesis of the central nervous system complications of both acute and chronic liver failure. Damage to astrocytes characterized by cell swelling (acute liver failure) or Alzheimer Type II astrocytosis ... Results of neuropathologic, spectroscopic, and neurochemical studies continue to confirm a major role for ammonia in the pathogenesis of the central nervous system complications of both acute and chronic liver failure. Damage to astrocytes characterized by cell swelling (acute liver failure) or Alzheimer Type II astrocytosis (chronic liver failure) can be readily reproduced by acute or chronic exposure of these cells in vitro to pathophysiologically relevant concentrations of ammonia. Furthermore, exposure of the brain or cultured astrocytes to ammonia results in similar alterations in expression of genes coding for key astrocytic proteins. Such proteins include the structural glial fibrillary acidic protein, glutamate transporters, and peripheral-type (mitochondrial) benzodiazepine receptors. Brain–blood ammonia concentration ratios (normally of the order of 2) are increased up to fourfold in liver failure and arterial blood ammonia concentrations are good predictors of cerebral herniation in patients with acute liver failure. Studies using 1H magnetic resonance spectroscopy in patients with chronic liver failure reveal a positive correlation between the severity of neuropsychiatric symptoms and brain concentrations of the brain ammonia-detoxification product glutamine. Increased intracellular glutamine may be a contributory cause of brain edema in hyperammonemia. Positron emission tomography studies using 13HN3 provide evidence of increased blood–brain ammonia transfer and brain ammonia utilization rates in patients with chronic liver failure. In addition to the use of nonabsorbable disaccharides and antibiotics to reduce gut ammonia production, new approaches to the treatment of hepatic encephalopathy by lowering of brain ammonia include the use of L-ornithine–L-aspartate and mild hypothermia. read more read less

Topics:

Hepatic encephalopathy (58%)58% related to the paper, Hyperammonemia (58%)58% related to the paper, Glial fibrillary acidic protein (53%)53% related to the paper
311 Citations
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Frequently asked questions

1. Can I write Metabolic Brain Disease in LaTeX?

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

2. Do you follow the Metabolic Brain Disease guidelines?

Yes, the template is compliant with the Metabolic Brain Disease 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 Metabolic Brain Disease?

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 Metabolic Brain Disease citation style.

4. Can I use the Metabolic Brain Disease 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 Metabolic Brain Disease.

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

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

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

7. Where can I find the template for the Metabolic Brain Disease?

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

SciSpace's Metabolic Brain Disease 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 Metabolic Brain Disease?

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 Metabolic Brain Disease?”

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

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

12. Is Metabolic Brain Disease'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 Metabolic Brain Disease?

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 Metabolic Brain Disease. 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 Metabolic Brain Disease?

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

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

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

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