Example of Current Neuropharmacology format
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Example of Current Neuropharmacology format Example of Current Neuropharmacology format Example of Current Neuropharmacology format Example of Current Neuropharmacology format
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Example of Current Neuropharmacology format Example of Current Neuropharmacology format Example of Current Neuropharmacology format Example of Current Neuropharmacology format
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open access Open Access ISSN: 1570159X e-ISSN: 18756190
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Current Neuropharmacology — Template for authors

Publisher: Bentham Science
Categories Rank Trend in last 3 yrs
Pharmacology (medical) #9 of 246 up up by 36 ranks
Psychiatry and Mental Health #18 of 502 up up by 55 ranks
Pharmacology #16 of 297 up up by 65 ranks
Neurology (clinical) #20 of 343 up up by 42 ranks
Neurology #10 of 156 up up by 30 ranks
journal-quality-icon Journal quality:
High
calendar-icon Last 4 years overview: 335 Published Papers | 3513 Citations
indexed-in-icon Indexed in: Scopus
last-updated-icon Last updated: 02/06/2020
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FAQ

Journal Performance & Insights

  • Impact Factor
  • CiteRatio
  • SJR
  • SNIP

Impact factor 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.

4.668

2% from 2018

Impact factor for Current Neuropharmacology from 2016 - 2019
Year Value
2019 4.668
2018 4.568
2017 4.068
2016 3.365
graph view Graph view
table view Table view

insights Insights

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

CiteRatio is a measure of average citations received per peer-reviewed paper published in the journal.

10.5

28% from 2019

CiteRatio for Current Neuropharmacology from 2016 - 2020
Year Value
2020 10.5
2019 8.2
2018 6.6
2017 5.6
2016 5.2
graph view Graph view
table view Table view

insights Insights

  • CiteRatio of this journal has increased by 28% in last years.
  • This journal’s CiteRatio is in the top 10 percentile category.

SCImago Journal Rank (SJR) measures weighted citations received by the journal. Citation weighting depends on the categories and prestige of the citing journal.

1.955

28% from 2019

SJR for Current Neuropharmacology from 2016 - 2020
Year Value
2020 1.955
2019 1.531
2018 1.49
2017 1.21
2016 1.385
graph view Graph view
table view Table view

insights Insights

  • SJR of this journal has increased by 28% in last years.
  • This journal’s SJR is in the top 10 percentile category.

Source Normalized Impact per Paper (SNIP) measures actual citations received relative to citations expected for the journal's category.

1.851

45% from 2019

SNIP for Current Neuropharmacology from 2016 - 2020
Year Value
2020 1.851
2019 1.277
2018 1.284
2017 1.015
2016 1.48
graph view Graph view
table view Table view

insights Insights

  • SNIP of this journal has increased by 45% in last years.
  • This journal’s SNIP is in the top 10 percentile category.

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CiteRatio: 6.1 | SJR: 1.333 | SNIP: 1.061
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CiteRatio: 4.3 | SJR: 1.395 | SNIP: 2.063

Current Neuropharmacology

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Bentham Science

Current Neuropharmacology

Current Neuropharmacology aims to provide current, timely and comprehensive reviews of all areas of neuropharmacology and related matters of neuroscience. The journal publishes reviews written by experts and leaders in the fields of molecular, cellular, and systems/behavioural...... Read More

Medicine

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Last updated on
02 Jun 2020
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ISSN
1570-159X
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Impact Factor
Medium - 0.944
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
Vancouver
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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 tunnel- ing regimes in superconducting microconstrictions: Excess current, charge imbalance, and supercurrent conversion. Phys. Rev. B. 2013;87(10):100510.

Top papers written in this journal

open accessOpen access Journal Article DOI: 10.2174/157015909787602823
Oxidative stress and neurodegenerative diseases: a review of upstream and downstream antioxidant therapeutic options.
Bayani Uttara1, Ajay Singh, Paolo Zamboni, Raghunath T. Mahajan

Abstract:

Free radicals are common outcome of normal aerobic cellular metabolism. In-built antioxidant system of body plays its decisive role in prevention of any loss due to free radicals. However, imbalanced defense mechanism of antioxidants, overproduction or incorporation of free radicals from environment to living system leads to ... Free radicals are common outcome of normal aerobic cellular metabolism. In-built antioxidant system of body plays its decisive role in prevention of any loss due to free radicals. However, imbalanced defense mechanism of antioxidants, overproduction or incorporation of free radicals from environment to living system leads to serious penalty leading to neuro-degeneration. Neural cells suffer functional or sensory loss in neurodegenerative diseases. Apart from several other environmental or genetic factors, oxidative stress (OS) leading to free radical attack on neural cells contributes calamitous role to neuro-degeneration. Though, oxygen is imperative for life, imbalanced metabolism and excess reactive oxygen species (ROS) generation end into a range of disorders such as Alzheimer's disease, Parkinson's disease, aging and many other neural disorders. Toxicity of free radicals contributes to proteins and DNA injury, inflammation, tissue damage and subsequent cellular apoptosis. Antioxidants are now being looked upon as persuasive therapeutic against solemn neuronal loss, as they have capability to combat by neutralizing free radicals. Diet is major source of antioxidants, as well as medicinal herbs are catching attention to be commercial source of antioxidants at present. Recognition of upstream and downstream antioxidant therapy to oxidative stress has been proved an effective tool in alteration of any neuronal damage as well as free radical scavenging. Antioxidants have a wide scope to sequester metal ions involved in neuronal plaque formation to prevent oxidative stress. In addition, antioxidant therapy is vital in scavenging free radicals and ROS preventing neuronal degeneration in post-oxidative stress scenario. read more read less

Topics:

Free-radical theory of aging (63%)63% related to the paper, Oxidative stress (59%)59% related to the paper, Antioxidant (50%)50% related to the paper
2,521 Citations
open accessOpen access Journal Article DOI: 10.2174/1570159X11311030006
Acetylcholinesterase Inhibitors: Pharmacology and Toxicology

Abstract:

Acetylcholinesterase is involved in the termination of impulse transmission by rapid hydrolysis of the neurotransmitter acetylcholine in numerous cholinergic pathways in the central and peripheral nervous systems. The enzyme inactivation, induced by various inhibitors, leads to acetylcholine accumulation, hyperstimulation of ... Acetylcholinesterase is involved in the termination of impulse transmission by rapid hydrolysis of the neurotransmitter acetylcholine in numerous cholinergic pathways in the central and peripheral nervous systems. The enzyme inactivation, induced by various inhibitors, leads to acetylcholine accumulation, hyperstimulation of nicotinic and muscarinic receptors, and disrupted neurotransmission. Hence, acetylcholinesterase inhibitors, interacting with the enzyme as their primary target, are applied as relevant drugs and toxins. This review presents an overview of toxicology and pharmacology of reversible and irreversible acetylcholinesterase inactivating compounds. In the case of reversible inhibitors being commonly applied in neurodegenerative disorders treatment, special attention is paid to currently approved drugs (donepezil, rivastigmine and galantamine) in the pharmacotherapy of Alzheimer's disease, and toxic carbamates used as pesticides. Subsequently, mechanism of irreversible acetylcholinesterase inhibition induced by organophosphorus compounds (insecticides and nerve agents), and their specific and nonspecific toxic effects are described, as well as irreversible inhibitors having pharmacological implementation. In addition, the pharmacological treatment of intoxication caused by organophosphates is presented, with emphasis on oxime reactivators of the inhibited enzyme activity administering as causal drugs after the poisoning. Besides, organophosphorus and carbamate insecticides can be detoxified in mammals through enzymatic hydrolysis before they reach targets in the nervous system. Carboxylesterases most effectively decompose carbamates, whereas the most successful route of organophosphates detoxification is their degradation by corresponding phosphotriesterases. read more read less

Topics:

Acetylcholinesterase (60%)60% related to the paper, Cholinergic (54%)54% related to the paper, Acetylcholine (54%)54% related to the paper, Nerve agent (54%)54% related to the paper, Galantamine (52%)52% related to the paper
1,218 Citations
open accessOpen access Journal Article DOI: 10.2174/157015908785777229
Functional neuroanatomy of the noradrenergic locus coeruleus: its roles in the regulation of arousal and autonomic function part I: principles of functional organisation.
E. R Samuels1, E Szabadi

Abstract:

The locus coeruleus (LC) is the major noradrenergic nucleus of the brain, giving rise to fibres innervating extensive areas throughout the neuraxis. Recent advances in neuroscience have resulted in the unravelling of the neuronal circuits controlling a number of physiological functions in which the LC plays a central role. Tw... The locus coeruleus (LC) is the major noradrenergic nucleus of the brain, giving rise to fibres innervating extensive areas throughout the neuraxis. Recent advances in neuroscience have resulted in the unravelling of the neuronal circuits controlling a number of physiological functions in which the LC plays a central role. Two such functions are the regulation of arousal and autonomic activity, which are inseparably linked largely via the involvement of the LC. The LC is a major wakefulness-promoting nucleus, resulting from dense excitatory projections to the majority of the cerebral cortex, cholinergic neurones of the basal forebrain, cortically-projecting neurones of the thalamus, serotoninergic neurones of the dorsal raphe and cholinergic neurones of the pedunculopontine and laterodorsal tegmental nucleus, and substantial inhibitory projections to sleep-promoting GABAergic neurones of the basal forebrain and ventrolateral preoptic area. Activation of the LC thus results in the enhancement of alertness through the innervation of these varied nuclei. The importance of the LC in controlling autonomic function results from both direct projections to the spinal cord and projections to autonomic nuclei including the dorsal motor nucleus of the vagus, the nucleus ambiguus, the rostroventrolateral medulla, the Edinger-Westphal nucleus, the caudal raphe, the salivatory nuclei, the paraventricular nucleus, and the amygdala. LC activation produces an increase in sympathetic activity and a decrease in parasympathetic activity via these projections. Alterations in LC activity therefore result in complex patterns of neuronal activity throughout the brain, observed as changes in measures of arousal and autonomic function. read more read less

Topics:

Dorsal motor nucleus (63%)63% related to the paper, Dorsal raphe nucleus (61%)61% related to the paper, Laterodorsal tegmental nucleus (61%)61% related to the paper, Basal forebrain (59%)59% related to the paper, Nucleus ambiguus (58%)58% related to the paper
527 Citations
open accessOpen access Journal Article DOI: 10.2174/1570159X13666150716165726
Alzheimer's disease: Targeting the Cholinergic System

Abstract:

Acetylcholine (ACh) has a crucial role in the peripheral and central nervous systems. The enzyme choline acetyltransferase (ChAT) is responsible for synthesizing ACh from acetyl-CoA and choline in the cytoplasm and the vesicular acetylcholine transporter (VAChT) uptakes the neurotransmitter into synaptic vesicles. Following d... Acetylcholine (ACh) has a crucial role in the peripheral and central nervous systems. The enzyme choline acetyltransferase (ChAT) is responsible for synthesizing ACh from acetyl-CoA and choline in the cytoplasm and the vesicular acetylcholine transporter (VAChT) uptakes the neurotransmitter into synaptic vesicles. Following depolarization, ACh undergoes exocytosis reaching the synaptic cleft, where it can bind its receptors, including muscarinic and nicotinic receptors. ACh present at the synaptic cleft is promptly hydrolyzed by the enzyme acetylcholinesterase (AChE), forming acetate and choline, which is recycled into the presynaptic nerve terminal by the high-affinity choline transporter (CHT1). Cholinergic neurons located in the basal forebrain, including the neurons that form the nucleus basalis of Meynert, are severely lost in Alzheimer's disease (AD). AD is the most ordinary cause of dementia affecting 25 million people worldwide. The hallmarks of the disease are the accumulation of neurofibrillary tangles and amyloid plaques. However, there is no real correlation between levels of cortical plaques and AD-related cognitive impairment. Nevertheless, synaptic loss is the principal correlate of disease progression and loss of cholinergic neurons contributes to memory and attention deficits. Thus, drugs that act on the cholinergic system represent a promising option to treat AD patients. read more read less

Topics:

Choline acetyltransferase (68%)68% related to the paper, Vesicular acetylcholine transporter (66%)66% related to the paper, Cholinergic neuron (66%)66% related to the paper, Cholinergic (65%)65% related to the paper, Choline transporter (64%)64% related to the paper
507 Citations
open accessOpen access Journal Article DOI: 10.2174/157015908785777210
Brain endothelial cell-cell junctions: how to "open" the blood brain barrier.
Svetlana M. Stamatovic1, Richard F. Keep, Anuska V. Andjelkovic

Abstract:

The blood-brain barrier (BBB) is a highly specialized structural and biochemical barrier that regulates the entry of blood-borne molecules into brain, and preserves ionic homeostasis within the brain microenvironment. BBB properties are primarily determined by junctional complexes between the cerebral endothelial cells. These... The blood-brain barrier (BBB) is a highly specialized structural and biochemical barrier that regulates the entry of blood-borne molecules into brain, and preserves ionic homeostasis within the brain microenvironment. BBB properties are primarily determined by junctional complexes between the cerebral endothelial cells. These complexes are comprised of tight and adherens junctions. Such restrictive angioarchitecture at the BBB reduces paracellular diffusion, while minimal vesicle transport activity in brain endothelial cells limits transcellular transport. Under normal conditions, this largely prevents the extravasation of large and small solutes (unless specific transporters are present) and prevents migration of any type of blood-borne cell. However, this is changed in many pathological conditions. There, BBB disruption ("opening") can lead to increased paracellular permeability, allowing entry of leukocytes into brain tissue, but also contributing to edema formation. In parallel, there are changes in the endothelial pinocytotic vesicular system resulting in the uptake and transfer of fluid and macromolecules into brain parenchyma. This review highlights the route and possible factors involved in BBB disruption in a variety of neuropathological disorders (e.g. CNS inflammation, Alzheimer's disease, Parkinson's disease, epilepsy). It also summarizes proposed signal transduction pathways that may be involved in BBB "opening". read more read less

Topics:

Drug delivery to the brain (61%)61% related to the paper, Blood–brain barrier (57%)57% related to the paper, Cell junction (55%)55% related to the paper, Paracellular transport (54%)54% related to the paper, Adherens junction (54%)54% related to the paper
395 Citations
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Current Neuropharmacology format uses Vancouver citation style.

Automatically format and order your citations and bibliography in a click.

SciSpace allows imports from all reference managers like Mendeley, Zotero, Endnote, Google Scholar etc.

Frequently asked questions

Absolutely not! With our tool, you can freely write without having to focus on LaTeX. You can write your entire paper as per the Current Neuropharmacology guidelines and autoformat it.

Yes. The template is fully compliant as per the guidelines of this journal. Our experts at SciSpace ensure that. Also, if there's any update in the journal format guidelines, we take care of it and include that in our algorithm.

Sure. We support all the top citation styles like APA style, MLA style, Vancouver style, Harvard style, Chicago style, etc. For example, in case of this journal, when you write your paper and hit autoformat, it will automatically update your article as per the Current Neuropharmacology citation style.

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Yup. You can choose the right template, copy-paste the contents from the word doc and click on auto-format. You'll have a publish-ready paper that you can download at the end.

A matter of seconds. Besides that, our intuitive editor saves a load of your time in writing and formating your manuscript.

One little Google search can get you the Word template for any journal. However, why do you need a Word template when you can write your entire manuscript on SciSpace, autoformat it as per Current Neuropharmacology's guidelines and download the same in Word, PDF and LaTeX formats? Try us out!.

Absolutely! You can do it using our intuitive editor. It's very easy. If you need help, you can always contact our support team.

SciSpace is an online tool for now. We'll soon release a desktop version. You can also request (or upvote) any feature that you think might be helpful for you and the research community in the feature request section once you sign-up with us.

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After you have written and autoformatted your paper, you can download it in multiple formats, viz., PDF, Docx and LaTeX.

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 those factors the review board, rejection rates, frequency of inclusion in indexes, Eigenfactor, etc. You must assess all the factors and then take the final call.

SHERPA/RoMEO Database

We have extracted this data from Sherpa Romeo to help our researchers understand the access level of this journal. The following table indicates the level of access a journal has as per Sherpa Romeo 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.

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

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

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After uploading your paper on SciSpace, you would see a button to request a journal submission service for Current Neuropharmacology.

Each submission service is completed within 4 - 5 working days.

Yes. SciSpace provides this functionality.

After signing up, you would need to import your existing references from Word or .bib file.

SciSpace would allow download of your references in Current Neuropharmacology Endnote style, according to bentham-science guidelines.

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