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Title of Journal: Acta Neuropathol

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Abbravation: Acta Neuropathologica

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Springer Berlin Heidelberg

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10.1007/978-3-642-19789-5_19

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1432-0533

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Nothing is wrong with descriptive papers

Authors: Werner Paulus
Publish Date: 2014/06/06
Volume: 128, Issue: 1, Pages: 159-159
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Abstract

When I read through a referee’s comments and I find the word “descriptive” or even “merely descriptive” in the initial sentences of the review I know that in the end the referee will very probably be negative and suggest that the paper be rejected Here “descriptive” apparently means boring oldfashioned static lowquality or simply dislike although semantically it indicates careful observation The “good” counterpart tends to be the word “mechanistic” meaning modelbased experimental studies that analyze pathogenesis although it is acknowledged that both “descriptive” and “mechanistic” are somewhat vaguely defined terms and there is no clear line of demarcation between the two 1 2In fact it has usually been the observational rather than the mechanistic study that has moved neuropathology and science in general ahead Furthermore surgical neuropathology as well as descriptive neuropathology research using human tissues has become more and more clinically relevant For example the most frequently cited and influential original papers published during the past 10 years in this journal have all been descriptive studies using human tissues such as those on TDP43 IDH1 and C9ORF72 In fact the Acta paper with the highest impact ever with more than 5400 citations so far is a classical descriptive paper based on autopsy brains namely the Braak and Braak staging of Alzheimer’s disease published in 1991Studies analyzing mechanisms of disease can tell a good story and may be more interesting while a descriptive study provides the facts The other way round descriptive studies may be boring and tend to overinterpret findings while the mechanistic approach helps to understand pathogenesis and eventually could result in new therapeutic approaches In other words mechanistic studies tend to be more entertaining while descriptive studies often tend to be more relevant This means that mechanistic studies need to be backed up by a reality check to make them relevant and neuropathology is in a unique position to undertake mechanistic studies AND verification using human specimens Studies on mechanisms without checking against the reality of human tissues may be an excellent science but may be in danger of becoming a kind of neuroscience in the clinical nirvana and do not represent neuropathology This selfconception is reflected in the subtitle of Acta Neuropathologica namely “Pathology and Mechanisms of Neurological Disease” Accordingly we love to publish excellent interesting AND relevant papers analyzing mechanisms of disease using in vitro or in vivo models and complemented by appropriate analyses of human tissues The same high priority is granted to excellent descriptive papers on tissuebased morphological or molecular features of neurological disease bearing an important clinical impact Mechanistic studies without verification in human tissues may be important and can also be published in this journal but their priority is somewhat lower if there are no apparent clinical implications The same is true for descriptive studies using animal models without providing experimental insight into pathogenesisNeuropathology is not merely neuroscience of neurological disease Neuropathology is identifying problems through the examination of human pathological material then designing experiments to test mechanistic hypotheses and finally confirming the relevance of these hypotheses by expert reexamination of human material Acta Neuropathologica is about to promote this view


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  1. Propagation of alpha-synuclein pathology: hypotheses, discoveries, and yet unresolved questions from experimental and human brain studies
  2. Nomenclature and nosology for neuropathologic subtypes of frontotemporal lobar degeneration: an update
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  4. Neuronal and glial accumulation of α- and β-synucleins in human lipidoses
  5. Tauopathy models and human neuropathology: similarities and differences
  6. Clinicopathologic characteristics of sporadic Japanese Creutzfeldt–Jakob disease classified according to prion protein gene polymorphism and prion protein type
  7. Refined brain tumor diagnostics and stratified therapies: the requirement for a multidisciplinary approach
  8. Lack of adrenoleukodystrophy protein enhances oligodendrocyte disturbance and microglia activation in mice with combined Abcd1 / Mag deficiency
  9. Oxidative damage in the olfactory system in Alzheimer's disease
  10. The multifaceted nature of amyloid precursor protein and its proteolytic fragments: friends and foes
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  12. Incidence of axonal injury in human brain tissue
  13. Valosin-containing protein and the pathogenesis of frontotemporal dementia associated with inclusion body myopathy
  14. Reduced astrocytic NF-κB activation by laquinimod protects from cuprizone-induced demyelination
  15. Common mutations of β-catenin in adamantinomatous craniopharyngiomas but not in other tumours originating from the sellar region
  16. Decreased pyramidal neuron size in Brodmann areas 44 and 45 in patients with autism
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