Journal of Neuropathology & Experimental Neurology:
In This Issue
Use It or Lose It.....
Mosole et al compared muscle biopsies from sedentary and very physically active seniors and observed reduced numbers of denervated fibers and higher percentages of re-innervated fibers in the active group. Their observations suggest that long-term physical activity promotes reinnervation of muscle fibers undergoing age-related denervation.
see page 284
Early Alzheimer-Related Dementia: Not Just Plaques and Tangles?
Iacono et al determined that the amount of insoluble amyloid-beta or tau in the brain at autopsy does not distinguish individuals with intact cognition from those with minimal cognitive impairment. Their results suggest that other protective or compensatory factors must also play a role.
see page 295
Neuronal Shrinkage After Stroke
Gemmell et al asked whether hippocampal pyramidal neurons undergo reduction in cell volume following stroke, and whether the changes are related to post-stroke dementia. Three-dimensional stereological analyses revealed reductions in CA4 and to a lesser extent CA3 neuron volumes in post-stroke patients developing dementia, but not in those recovering with good cognition. This suggests that neuronal atrophy without cell loss may contribute to dementing disorders.
see page 305
The Cerebellum Again Provides No Clues to the Pathogenesis of SIDS
In the continued quest to understand the pathophysiologic basis of SIDS, Müller-Starck et al examined a sensitive measure of hypoxia in the cerebellum. Similar to the lack of Purkinje cell changes in SIDS, no changes in microvessel length density were found.
see page 312
Perinatal Ischemia and Epilepsy
Schiering, de Haan et al evaluated hippocampal pathology in deceased full-term asphyxiated infants with or without seizures to assess effects of perinatal asphyxia on subsequent seizure development. Cases with seizures displayed neuronal alterations, inflammatory changes and blood-brain barrier disruption compared to cases without seizures and other controls thereby implicating their roles in the pathogenesis of post-hypoxic seizures.
see page 324
A Transient Cortical Motor Neuronopathy in Chronic EAE
Using neuron-specific markers with immunohistochemistry, Burns et al found that although there was no cortical motor neuron loss over the course of myelin oligodendrocyte glycoprotein-induced EAE there were pre-synaptic neuron perturbations in neocortical neuron layer V. These alterations correlated with cortical demyelination but not extent of inflammation in corticospinal tracts and corpus callosum. Their results parallel neuroimaging results in MS patients and indicate that there are reversible cortical neuron perturbations that may have pathophysiological significance in patients with chronic demyelinating diseases.
see page 335
With an Eye on Trauma
Using a mouse model of traumatic brain injury the authors observed demyelination, increased cellularity and decreased diameters of the optic nerves, retinal thinning and decreased cellularity of the retinal ganglion cell layer. Electroretinography and spectral-domain optical coherence tomography data correlated with the histological findings.
see page 345
Similarity Between HIV-Associated Dementia and Alzheimer Disease Amyloidosis?
Based on prior evidence that activation of chemokine CCL4/MIP-1β has a detrimental effect on neuronal integrity in HIV-associated dementia, the authors studied CCL4 expression in the APP/PS1 double-transgenic mouse model of AD cerebral amyloidosis. They found overexpression of CCL4 mRNA and protein, and increased expression of its putative transcription factor ATF3. They conclude that CCL4 may contribute to the neuropathologic progression of amyloid deposition in AD.
see page 362
© 2014 by American Association of Neuropathologists, Inc.