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Example of Acta Neuropathologica Communications format Example of Acta Neuropathologica Communications format Example of Acta Neuropathologica Communications format Example of Acta Neuropathologica Communications format Example of Acta Neuropathologica Communications format Example of Acta Neuropathologica Communications format Example of Acta Neuropathologica Communications format Example of Acta Neuropathologica Communications format Example of Acta Neuropathologica Communications format Example of Acta Neuropathologica Communications format Example of Acta Neuropathologica Communications format Example of Acta Neuropathologica Communications format Example of Acta Neuropathologica Communications format Example of Acta Neuropathologica Communications format Example of Acta Neuropathologica Communications format Example of Acta Neuropathologica Communications format Example of Acta Neuropathologica Communications format Example of Acta Neuropathologica Communications format
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Example of Acta Neuropathologica Communications format Example of Acta Neuropathologica Communications format Example of Acta Neuropathologica Communications format Example of Acta Neuropathologica Communications format Example of Acta Neuropathologica Communications format Example of Acta Neuropathologica Communications format Example of Acta Neuropathologica Communications format Example of Acta Neuropathologica Communications format Example of Acta Neuropathologica Communications format Example of Acta Neuropathologica Communications format Example of Acta Neuropathologica Communications format Example of Acta Neuropathologica Communications format Example of Acta Neuropathologica Communications format Example of Acta Neuropathologica Communications format Example of Acta Neuropathologica Communications format Example of Acta Neuropathologica Communications format Example of Acta Neuropathologica Communications format Example of Acta Neuropathologica Communications format
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Acta Neuropathologica Communications — Template for authors

Publisher: Springer
Guideline source
Categories Rank Trend in last 3 yrs
Pathology and Forensic Medicine #10 of 191 down down by 4 ranks
Neurology (clinical) #37 of 343 down down by 21 ranks
Cellular and Molecular Neuroscience #20 of 88 down down by 12 ranks
journal-quality-icon Journal quality:
High
calendar-icon Last 4 years overview: 632 Published Papers | 5181 Citations
indexed-in-icon Indexed in: Scopus
last-updated-icon Last updated: 17/06/2020
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Related Journals

open access Open Access
recommended Recommended

Acta Neuropathologica

Springer

Quality:  
High
CiteRatio: 23.3
SJR: 7.183
SNIP: 3.099
Indexed in: Scopus Last updated: 16/07/2020
open access Open Access
recommended Recommended

Nature Reviews Neurology

Nature

Quality:  
High
CiteRatio: 29.5
SJR: 7.271
SNIP: 5.939
Indexed in: Scopus Last updated: 08/06/2020
open access Open Access

Brain Imaging and Behavior

Springer

Quality:  
High
CiteRatio: 6.0
SJR: 1.239
SNIP: 1.096
Indexed in: Scopus Last updated: 21/06/2020
open access Open Access
recommended Recommended

Journal of Neurodevelopmental Disorders

Springer

Quality:  
High
CiteRatio: 5.9
SJR: 1.431
SNIP: 1.344
Indexed in: Scopus Last updated: 08/06/2020

Journal Performance & Insights

CiteRatio

SCImago Journal Rank (SJR)

Source Normalized Impact per Paper (SNIP)

A measure of average citations received per peer-reviewed paper published in the journal.

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.

8.2

4% from 2019

CiteRatio for Acta Neuropathologica Communications from 2016 - 2020
Year Value
2020 8.2
2019 7.9
2018 8.3
2017 10.4
2016 7.6
graph view Graph view
table view Table view

3.131

10% from 2019

SJR for Acta Neuropathologica Communications from 2016 - 2020
Year Value
2020 3.131
2019 2.845
2018 3.279
2017 2.683
2016 2.45
graph view Graph view
table view Table view

1.18

11% from 2019

SNIP for Acta Neuropathologica Communications from 2016 - 2020
Year Value
2020 1.18
2019 1.331
2018 1.77
2017 1.266
2016 1.522
graph view Graph view
table view Table view

insights Insights

  • CiteRatio of this journal has increased by 4% in last years.
  • This journal’s CiteRatio is in the top 10 percentile category.

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 decreased by 11% in last years.
  • This journal’s SNIP is in the top 10 percentile category.

Acta Neuropathologica Communications

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Springer

Acta Neuropathologica Communications

Approved by publishing and review experts on SciSpace, this template is built as per for Acta Neuropathologica Communications formatting guidelines as mentioned in Springer author instructions. The current version was created on and has been used by 766 authors to write and format their manuscripts to this journal.

i
Last updated on
16 Jun 2020
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ISSN
1606-8610
i
Open Access
Yes
i
Sherpa RoMEO Archiving Policy
White faq
i
Plagiarism Check
Available via Turnitin
i
Endnote Style
Download Available
i
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/S40478-015-0203-5 •
Induction of a common microglia gene expression signature by aging and neurodegenerative conditions: a co-expression meta-analysis
Inge R. Holtman1, Divya Raj1, Jeremy A. Miller2, Wandert Schaafsma1, Zhuoran Yin1, Nieske Brouwer1, Paul D. Wes3, Thomas Möller3, Marie Orre4, Willem Kamphuis4, Elly M. Hol4, Elly M. Hol5, Elly M. Hol6, Erik Boddeke1, Bart J. L. Eggen1 •
University Medical Center Groningen1, Allen Institute for Brain Science2, Lundbeck3, Royal Netherlands Academy of Arts and Sciences4, University of Amsterdam5, Utrecht University6
23 May 2015 - Acta neuropathologica communications

Abstract:

Microglia are tissue macrophages of the central nervous system that monitor brain homeostasis and react upon neuronal damage and stress. Aging and neurodegeneration induce a hypersensitive, pro-inflammatory phenotype, referred to as primed microglia. To determine the gene expression signature of priming, the transcriptomes of... Microglia are tissue macrophages of the central nervous system that monitor brain homeostasis and react upon neuronal damage and stress. Aging and neurodegeneration induce a hypersensitive, pro-inflammatory phenotype, referred to as primed microglia. To determine the gene expression signature of priming, the transcriptomes of microglia in aging, Alzheimer’s disease (AD), and amyotrophic lateral sclerosis (ALS) mouse models were compared using Weighted Gene Co-expression Network Analysis (WGCNA). A highly consistent consensus transcriptional profile of up-regulated genes was identified, which prominently differed from the acute inflammatory gene network induced by lipopolysaccharide (LPS). Where the acute inflammatory network was significantly enriched for NF-κB signaling, the primed microglia profile contained key features related to phagosome, lysosome, antigen presentation, and AD signaling. In addition, specific signatures for aging, AD, and ALS were identified. Microglia priming induces a highly conserved transcriptional signature with aging- and disease-specific aspects. read more read less

Topics:

Neuroinflammation (60%)60% related to the paper, Microglia (54%)54% related to the paper, Neurodegeneration (53%)53% related to the paper
View PDF
443 Citations
open accessOpen access • Journal Article • DOI: 10.1186/S40478-014-0135-5 •
Inconsistencies and controversies surrounding the amyloid hypothesis of Alzheimer's disease.
Gary P. Morris1, Gary P. Morris2, Ian A. Clark3, Bryce Vissel1, Bryce Vissel2 •
University of New South Wales1, Garvan Institute of Medical Research2, Australian National University3
18 Sep 2014 - Acta neuropathologica communications

Abstract:

The amyloid hypothesis has driven drug development strategies for Alzheimer's disease for over 20 years. We review why accumulation of amyloid-beta (Aβ) oligomers is generally considered causal for synaptic loss and neurodegeneration in AD. We elaborate on and update arguments for and against the amyloid hypothesis with new d... The amyloid hypothesis has driven drug development strategies for Alzheimer's disease for over 20 years. We review why accumulation of amyloid-beta (Aβ) oligomers is generally considered causal for synaptic loss and neurodegeneration in AD. We elaborate on and update arguments for and against the amyloid hypothesis with new data and interpretations, and consider why the amyloid hypothesis may be failing therapeutically. We note several unresolved issues in the field including the presence of Aβ deposition in cognitively normal individuals, the weak correlation between plaque load and cognition, questions regarding the biochemical nature, presence and role of Aβ oligomeric assemblies in vivo, the bias of pre-clinical AD models toward the amyloid hypothesis and the poorly explained pathological heterogeneity and comorbidities associated with AD. We also illustrate how extensive data cited in support of the amyloid hypothesis, including genetic links to disease, can be interpreted independently of a role for Aβ in AD. We conclude it is essential to expand our view of pathogenesis beyond Aβ and tau pathology and suggest several future directions for AD research, which we argue will be critical to understanding AD pathogenesis. read more read less

Topics:

Amyloid beta (62%)62% related to the paper, Biochemistry of Alzheimer's disease (61%)61% related to the paper, Amyloid precursor protein (53%)53% related to the paper
View PDF
395 Citations
open accessOpen access • Journal Article • DOI: 10.1186/S40478-016-0315-6 •
An autoradiographic evaluation of AV-1451 Tau PET in dementia.
Val J. Lowe1, Geoffry L. Curran1, Ping Fang1, Amanda M. Liesinger1, Keith A. Josephs1, Joseph E. Parisi1, Kejal Kantarci1, Bradley F. Boeve1, Mukesh K. Pandey1, Tyler J. Bruinsma1, David S. Knopman1, David T.W. Jones1, Leonard Petrucelli1, Casey Cook1, Neill R. Graff-Radford1, Dennis W. Dickson1, Ronald C. Petersen1, Clifford R. Jack1, Melissa E. Murray1 •
Mayo Clinic1
13 Jun 2016 - Acta neuropathologica communications

Abstract:

It is essential to determine the specificity of AV-1451 PET for tau in brain imaging by using pathological comparisons. We performed autoradiography in autopsy-confirmed Alzheimer disease and other neurodegenerative disorders to evaluate the specificity of AV-1451 binding for tau aggregates. Tissue samples were selected that ... It is essential to determine the specificity of AV-1451 PET for tau in brain imaging by using pathological comparisons. We performed autoradiography in autopsy-confirmed Alzheimer disease and other neurodegenerative disorders to evaluate the specificity of AV-1451 binding for tau aggregates. Tissue samples were selected that had a variety of dementia-related neuropathologies including Alzheimer disease, primary age-related tauopathy, tangle predominant dementia, non-Alzheimer disease tauopathies, frontotemporal dementia, parkinsonism, Lewy body disease and multiple system atrophy (n = 38). Brain tissue sections were stained for tau, TAR DNA-binding protein-43, and α-synuclein and compared to AV-1451 autoradiography on adjacent sections. AV-1451 preferentially localized to neurofibrillary tangles, with less binding to areas enriched in neuritic pathology and less mature tau. The strength of AV-1451 binding with respect to tau isoforms in various neurodegenerative disorders was: 3R + 4R tau (e.g., AD) > 3R tau (e.g., Pick disease) or 4R tau. Only minimal binding of AV-1451 to TAR DNA-binding protein-43 positive regions was detected. No binding of AV-1451 to α-synuclein was detected. “Off-target” binding was seen in vessels, iron-associated regions, substantia nigra, calcifications in the choroid plexus, and leptomeningeal melanin. Reduced AV-1451 binding in neuritic pathology compared to neurofibrillary tangles suggests that the maturity of tau pathology may affect AV-1451 binding and suggests complexity in AV-1451 binding. Poor association of AV-1451 with tauopathies that have preferential accumulation of either 4R tau or 3R tau suggests limited clinical utility in detecting these pathologies. In contrast, for disorders associated with 3R + 4R tau, such as Alzheimer disease, AV-1451 binds tau avidly but does not completely reflect the early stage tau progression suggested by Braak neurofibrillary tangle staging. AV-1451 binding to TAR DNA-binding protein-43 or TAR DNA-binding protein-43 positive regions can be weakly positive. Clinical use of AV-1451 will require a familiarity with distinct types of “off-target” binding. read more read less

Topics:

Neurofibrillary tangle (68%)68% related to the paper, Pick's disease (63%)63% related to the paper, Tauopathy (60%)60% related to the paper, Progressive supranuclear palsy (59%)59% related to the paper, Alzheimer's disease (56%)56% related to the paper
View PDF
391 Citations
open accessOpen access • Journal Article • DOI: 10.1186/S40478-018-0515-3 •
White matter changes in Alzheimer's disease: a focus on myelin and oligodendrocytes.
Sara Ebrahimi Nasrabady1, Batool Rizvi1, James E. Goldman1, Adam M. Brickman1 •
Columbia University1
02 Mar 2018 - Acta neuropathologica communications

Abstract:

Alzheimer’s disease (AD) is conceptualized as a progressive consequence of two hallmark pathological changes in grey matter: extracellular amyloid plaques and neurofibrillary tangles. However, over the past several years, neuroimaging studies have implicated micro- and macrostructural abnormalities in white matter in the risk... Alzheimer’s disease (AD) is conceptualized as a progressive consequence of two hallmark pathological changes in grey matter: extracellular amyloid plaques and neurofibrillary tangles. However, over the past several years, neuroimaging studies have implicated micro- and macrostructural abnormalities in white matter in the risk and progression of AD, suggesting that in addition to the neuronal pathology characteristic of the disease, white matter degeneration and demyelination may be also important pathophysiological features. Here we review the evidence for white matter abnormalities in AD with a focus on myelin and oligodendrocytes, the only source of myelination in the central nervous system, and discuss the relationship between white matter changes and the hallmarks of Alzheimer’s disease. We review several mechanisms such as ischemia, oxidative stress, excitotoxicity, iron overload, Aβ toxicity and tauopathy, which could affect oligodendrocytes. We conclude that white matter abnormalities, and in particular myelin and oligodendrocytes, could be mechanistically important in AD pathology and could be potential treatment targets. read more read less

Topics:

White matter (63%)63% related to the paper, Grey matter (59%)59% related to the paper, Tauopathy (55%)55% related to the paper, Alzheimer's disease (53%)53% related to the paper, Myelin (52%)52% related to the paper
View PDF
359 Citations
open accessOpen access • Journal Article • DOI: 10.1186/S40478-017-0488-7 •
What is the evidence that tau pathology spreads through prion-like propagation?
Amrit Mudher1, Morvane Colin2, Simon Dujardin3, Miguel Medina, Ilse Dewachter4, Seyedeh Maryam Alavi Naini5, Eva-Maria Mandelkow, Eckhard Mandelkow, Luc Buée2, Michel Goedert6, Jean Pierre Brion7 •
University of Southampton1, university of lille2, Harvard University3, University of Hasselt4, Pierre-and-Marie-Curie University5, Laboratory of Molecular Biology6, Université libre de Bruxelles7
19 Dec 2017 - Acta neuropathologica communications

Abstract:

Emerging experimental evidence suggests that the spread of tau pathology in the brain in Tauopathies reflects the propagation of abnormal tau species along neuroanatomically connected brain areas. This propagation could occur through a “prion-like” mechanism involving transfer of abnormal tau seeds from a “donor cell” to a “r... Emerging experimental evidence suggests that the spread of tau pathology in the brain in Tauopathies reflects the propagation of abnormal tau species along neuroanatomically connected brain areas. This propagation could occur through a “prion-like” mechanism involving transfer of abnormal tau seeds from a “donor cell” to a “recipient cell” and recruitment of normal tau in the latter to generate new tau seeds. This review critically appraises the evidence that the spread of tau pathology occurs via such a “prion-like” mechanism and proposes a number of recommendations for directing future research. Recommendations for definitions of frequently used terms in the tau field are presented in an attempt to clarify and standardize interpretation of research findings. Molecular and cellular factors affecting tau aggregation are briefly reviewed, as are potential contributions of physiological and pathological post-translational modifications of tau. Additionally, the experimental evidence for tau seeding and “prion-like” propagation of tau aggregation that has emerged from cellular assays and in vivo models is discussed. Propagation of tau pathology using “prion-like” mechanisms is expected to incorporate several steps including cellular uptake, templated seeding, secretion and intercellular transfer through synaptic and non-synaptic pathways. The experimental findings supporting each of these steps are reviewed. The clinical validity of these experimental findings is then debated by considering the supportive or contradictory findings from patient samples. Further, the role of physiological tau release in this scenario is examined because emerging data shows that tau is secreted but the physiological function (if any) of this secretion in the context of propagation of pathological tau seeds is unclear. Bona fide prions exhibit specific properties, including transmission from cell to cell, tissue to tissue and organism to organism. The propagation of tau pathology has so far not been shown to exhibit all of these steps and how this influences the debate of whether or not abnormal tau species can propagate in a “prion-like” manner is discussed. The exact nature of tau seeds responsible for propagation of tau pathology in human tauopathies remains controversial; it might be tightly linked to the existence of tau strains stably propagating peculiar patterns of neuropathological lesions, corresponding to the different patterns seen in human tauopathies. That this is a property shared by all seed-competent tau conformers is not yet firmly established. Further investigation is also required to clarify the relationship between propagation of tau aggregates and tau-induced toxicity. Genetic variants identified as risks factors for tauopathies might play a role in propagation of tau pathology, but many more studies are needed to document this. The contribution of selective vulnerability of neuronal populations, as an alternative to prion-like mechanisms to explain spreading of tau pathology needs to be clarified. Learning from the prion field will be helpful to enhance our understanding of propagation of tau pathology. Finally, development of better models is expected to answer some of these key questions and allow for the testing of propagation-centred therapies. read more read less
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245 Citations
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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 Acta Neuropathologica Communications?

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 Acta Neuropathologica Communications. 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 Acta Neuropathologica Communications?

The 5 most common citation types in order of usage for Acta Neuropathologica Communications 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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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 Acta Neuropathologica Communications Endnote style according to Elsevier guidelines.

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