Vulnerability of small GABAergic neurons to human β-amyloid pentapeptide
Autor: | Magdolna Pakaski, Zoltan Farkas, Peter Kasa, Monika Forgon, Henrietta Papp, Marta Zarandi, Botond Penke |
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Rok vydání: | 1998 |
Předmět: |
Amyloid
Population Drug Resistance Apoptosis Peptide Biology Image Processing Computer-Assisted medicine Animals Humans Senile plaques education Molecular Biology gamma-Aminobutyric Acid Ultrasonography Neurons chemistry.chemical_classification education.field_of_study Basal forebrain Amyloid beta-Peptides General Neuroscience Neurodegeneration medicine.disease Immunohistochemistry Peptide Fragments Rats Amino acid Cell biology chemistry Microscopy Electron Scanning GABAergic Neurology (clinical) Neuroscience Developmental Biology |
Zdroj: | Brain Research. 796:239-246 |
ISSN: | 0006-8993 |
Popis: | b-Amyloid peptide A b , the principal component of senile plaques in Alzheimer's disease, has been found to be neurotoxic. The role of A b in the deficits of the GABAergic system in patients with Alzheimer's disease is unclear. It has been suggested that the cytotoxic activity of A b is localized to amino acid residues 25-35 of this peptide, which contains a total of 42 amino acid residues. We now report . . that the short amyloid peptide fragments corresponding to amino acids 31-35 Ab 31-35 and 34-39 Ab 34-39 are also toxic in vitro to the small GABAergic neuron population of basal forebrain cultures. Morphological changes were accompanied by an increased number of varicosities localized on the processes of the GABA-immunoreactive neurons and by the appearance of round cells without processes. The neurodegeneration was confirmed by means of scanning electron microscopy. Quantification of the morphological findings by image analysis demonstrated a size-related dependence of the degeneration of GABAergic neurons. The results suggest that fragments of A b shorter than A b 25-35 may exert cytotoxic action and demonstrate the toxicity of these A b fragments in decreasing the number of small GABAergic neurons. q 1998 Elsevier Science B.V. All rights reserved. |
Databáze: | OpenAIRE |
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