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Hippocampal Pathology (hippocampal + pathology)

Distribution by Scientific Domains

Medical Sciences	83%

Selected Abstracts

Hippocampal Pathology in the Human Neuronal Ceroid-Lipofuscinoses: Distinct Patterns of Storage Deposition, Neurodegeneration and Glial Activation

BRAIN PATHOLOGY, Issue 4 2004
Jaana Tyynelä
The neuronal ceroid-lipofuscinoses (NCLs) are recessively inherited lysosomal storage diseases, currently classified into 8 forms (CLN1-CLN8). Collectively, the NCLs constitute the most common group of progressive encephalopathies of childhood, and present with visual impairment, psychomotor deterioration and severe seizures. Despite recent identification of the underlying disease genes, the mechanisms leading to neurodegeneration and epilepsy in the NCLs remain poorly understood. To investigate these events, we examined the patterns of storage deposition, neurodegeneration, and glial activation in the hippocampus of patients with CLN1, CLN2, CLN3, CLN5 and CLN8 using histochemistry and immunohistochemistry. These different forms of NCL shared distinct patterns of neuronal degeneration in the hippocampus, with heavy involvement of sectors CA2-CA4 but relative sparing of CA1. This selective pattern of degeneration was also observed in immunohistochemically identified interneurons, which exhibited a graded severity of loss according to phenotype, with calretinin-positive interneurons relatively spared. Furthermore, glial activation was also regionally specific, with microglial activation most pronounced in areas of greatest neuronal loss, and astrocyte activation prominent in areas where neuronal loss was less evident. In conclusion, the NCLs share a common pattern of selective hippocampal pathology, distinct from that seen in the majority of temporal lobe epilepsies. [source]

Workshop W03: Hippocampal Pathology in Epilepsy

BRAIN PATHOLOGY, Issue 4 2000
Article first published online: 5 APR 200
No abstract is available for this article. [source]

Stroke in the developing brain and intractable epilepsy: effect of timing on hippocampal sclerosis

DEVELOPMENTAL MEDICINE & CHILD NEUROLOGY, Issue 9 2003
Waney Squier FRCP FRC Path
A detailed study was made of the pathology of specimens removed by hemispherectomy for the treatment of intractable epilepsy in children with unilateral middle cerebral artery stroke. Neuropathological criteria were used to differentiate strokes that occurred in early intrauterine development (before 28 weeks gestational age) from those occurring in the last trimester, at birth, or after birth: 19 children had early strokes and 21 late. There was no difference in seizure history or occurrence of febrile convulsions in these two groups. Hippocampal tissue was available in 20 patients; pathology in the hippocampus, remote from the infarcted area, showed a marked difference between early-onset and late-onset groups. Hippocampal sclerosis was uncommon in children with early-onset strokes but developed in most of the children whose strokes were of later origin. However, hippocampal sclerosis was more closely related to a clinical history of a late initial precipitating insult irrespective of infarct timing. These findings demonstrate the changing vulnerability of the developing brain and show that hippocampal pathology is more closely related to the timing of an insult than seizure history or the occurrence of febrile convulsions. [source]

Hippocampal structure and the action of cholinomimetic drugs

DRUG DEVELOPMENT RESEARCH, Issue 3 2002
John G. Csernansky
Abstract Cholinomimetic drugs have become the clinical standard for the treatment of patients with dementia of the Alzheimer type (DAT). However, uncertainty remains as to the proportion of patients that respond to such drugs, and how one might predict the capacity for response before treatment is begun. The thesis of the present review is that the neuroanatomical integrity of the hippocampus determines, at least in part, the capacity of DAT patients to respond to cholinomimetic drugs. Neuroimaging studies suggest that volume losses and other neuroanatomical deformities of the hippocampus are common in patients with even mild DAT. Moreover, more severe neuroanatomical deformities of the hippocampus are associated with more severe dementia symptoms and more rapid clinical decline. Animal research, including studies of cholinergic antagonists, glutamatergic antagonists, hippocampal lesions, and animals with mutant amyloid precursor protein genes, demonstrate that behavioral abnormalities similar to those found in DAT patients, especially those related to memory, are associated with hippocampal pathology. Cholinomimetic drugs, in particular, the cholinesterase inhibitors, have been shown to reverse some but not all of these behavioral abnormalities. More research is needed in DAT patients to determine whether an analysis of hippocampal structure or function can reliably predict the outcome of treatment with cholinomimetic drugs. Further work in animals is also needed to determine the limitations of cholinomimetic drugs for reversing various types of cognitive deficits, and to develop and test other pharmacological strategies for the treatment of DAT. Drug Dev. Res. 56:531,540, 2002. © 2002 Wiley-Liss, Inc. [source]

Hypothermia treatment potentiates ERK1/2 activation after traumatic brain injury

EUROPEAN JOURNAL OF NEUROSCIENCE, Issue 4 2007
Coleen M. Atkins
Abstract Traumatic brain injury (TBI) results in significant hippocampal pathology and hippocampal-dependent memory loss, both of which are alleviated by hypothermia treatment. To elucidate the molecular mechanisms regulated by hypothermia after TBI, rats underwent moderate parasagittal fluid-percussion brain injury. Brain temperature was maintained at normothermic or hypothermic temperatures for 30 min prior and up to 4 h after TBI. The ipsilateral hippocampus was assayed with Western blotting. We found that hypothermia potentiated extracellular signal-regulated kinase 1/2 (ERK1/2) activation and its downstream effectors, p90 ribosomal S6 kinase (p90RSK) and the transcription factor cAMP response element-binding protein. Phosphorylation of another p90RSK substrate, Bad, also increased with hypothermia after TBI. ERK1/2 regulates mRNA translation through phosphorylation of mitogen-activated protein kinase-interacting kinase 1 (Mnk1) and the translation factor eukaryotic initiation factor 4E (eIF4E). Hypothermia also potentiated the phosphorylation of both Mnk1 and eIF4E. Augmentation of ERK1/2 activation and its downstream signalling components may be one molecular mechanism that hypothermia treatment elicits to improve functional outcome after TBI. [source]