Neuropathology and Applied Neurobiology
© British Neuropathological Society
Edited By: Dr Stephen Wharton
Impact Factor: 4.837
ISI Journal Citation Reports © Ranking: 2012: 8/77 (Pathology); 19/193 (Clinical Neurology); 45/252 (Neurosciences)
Online ISSN: 1365-2990
Read Stephen Wharton's choice of top articles FREE online:
Review: The human premotor oculomotor brainstem system - can it help to understand oculomotor symptoms in Huntington's disease?
U. Rüb, H. Heinsen, E. R. Brunt, B. Landwehrmeyer et al
Rüb et al review the function neuroanatomy and involvement of the premotor oculomotor brainstem system in Huntington's disease.
Lentivirus Tau (P301S) expression in adult amyloid precursor protein (APP)-transgenic mice leads to tangle formation
M. Osinde, F. Clavaguera, R. May-Nass et al
Using a lentiviral system to over-express mutant tau in an APP transgenic model, Osinde et al show that APP or Aβpromotes tau pathology in adult brain, independently of early developmental mechanisms.
Diagnostic value of WT1 in neuroepithelial tumours
J. Schittenhelm, R. Beschorner, P. Simon et al
This paper reports a comprehensive survey of WT1 expression in human gliomas. The work suggests that WT1 may have a role in the development of brain tumours and be of differential diagnostic value.
pH measurement as quality control on human post mortem brain tissue: a study of the BrainNet Europe consortium
C. M. Monoranu, M. Apfelbacher, E. Grünblatt et al
This study from the BrainNet Europe Consortium adds to the work from this group contributing to improved standards in brain banking. This paper shows the value of tissue pH, which is dependent on pre-mortem agonal state and ischaemia, as a quality measure for brain banking.
Microcalcification after excitotoxicity is enhanced in transgenic mice expressing parvalbumin in all neurones, may commence in neuronal mitochondria and undergoes structural modifications over time
W. Maetzler, H. Stünitz, K. Bendfeldt et al
Microcalcification occurs in several neurodegenerative diseases and neuronal injury states. Maetzler et al have studied microcalcification in an excitotoxicity model. The regulation of calcium shuttling into calcium stores is relevant to the ability of neurones to respond to injury.
Pathogenesis and molecular targeted therapy of spinal and bulbar muscular atrophy
H. Adachi, M. Waza, M. Katsuno, F. Tanaka, M. Doyu, G. Sobue
This review discusses the latest in the molecular pathology and pathogenesis of SBMA. The authors discuss novel approaches to therapy and biomarker development based on advances in the understanding of pathologenesis.
Classical sheep transmissible spongiform encephalopathies: pathogenesis, pathological phenotypes and clinical disease
M. Jeffrey, L. González
This review discusses the relationship of the varied molecular phenotypes of sheep scrapie to strain diversity and clinical manifestations. The authors also review the latest state of knowledge of peripheral nervous system and lymphoreticular involvement, which are important for disease transmission and food safety.
Genetic intratumour heterogeneity in high-grade brain tumours is associated with telomere-dependent mitotic instability
C. Glanz, et al
An investigation of the mechanisms by which complex chromosomal abnormalities develop in glioblastoma, showing that telomere-dependent abnormal chromosome segregation at mitosis is a common occurrence.
Expression of the endoplasmic reticulum stress response marker, BiP, in the central nervous system of HIV-positive individuals
K. A. Lindl, C. Akay, Y. Wang, M. G. White, K. L. Jordan-Sciutto
This paper shows that there is an up-regulation of a master regulator and an initiator of the endoplasmic reticulum stress response pathway, suggesting that the ER stress response plays a role in HIV-related neurocognitive impairment.
Limbic structures are prone to age-related impairments in proteasome activity and neuronal ubiquitinated inclusions in SAMP10 mouse: a model of cerebral degeneration
A. Shimada, H. Keino, N. Kawamura, Y. Chiba, M. Hosokawa
Ubiquitinated inclusion formation in a senescence accelerated model system, showing the importance of proteasomal impairment for neurodegeneration. Regionally selective proteasomal impairment in this model explains the regional susceptibility to inclusion formation.