caa a22 4500 465768822 CHVBK 20180323111923.0 cr unu---uuuuu 170327e19901201xx s 000 0 eng 10.1007/BF00334497 doi (NATIONALLICENCE)springer-10.1007/BF00334497 Ferritin is a component of the neuritic (senile) plaque in Alzheimer dementia [Elektronische Daten] [I. Grundke-Iqbal, J. Fleming, Y. Tung, H. Lassmann, K. Iqbal, J. Joshi] Summary: A strong immunoreactivity for ferritin was observed in the neuritic (senile) plaques in Alzheimer's disease hippocampus. The ferritin accumulation was almost exclusively associated with the microglia, which appeared to have proliferated greatly. These cells were also positive for HLA-DR, a putative marker for reactive microglia. In contrast, in the diffuse plaques, which were without neuritic pathology, the ferritin-stained microglia appeared to be normal. Microglia were seen frequently in contact with neurons undergoing neurofibrillary changes but only the tangles in the extracellular space were ferritin positive. No ferritin was detected, by Western blots, in paired helical filaments isolated from Alzheimer's disease brain, suggesting that ferritin was most likely weakly associated with and was not a constituent of these fibrils. No correlation between increased ferritin/microglia activity and blood-brain barrier leakage was detected. Ferritin, an iron-storage protein, might have a role in the formation of amyloid through the action of free radicals generated during the release of iron from the ferritin molecule. Alternatively, the ferritin/microglia system might be secondarily involved in the removal and processing of the amyloid. Springer-Verlag, 1990 Microglia nationallicence Amyloid nationallicence Ferritin nationallicence Paired helical filaments nationallicence Alzheimer's disease nationallicence Grundke-Iqbal I. New York State Institute for Basic Research in Developmental Disabilities, 1050 Forest Hill Road, 10314, Staten Island, NY, USA aut Fleming J. Department of Biochemistry, University of Tennessee, 37996-0840, Knoxville, TN, USA aut Tung Y. New York State Institute for Basic Research in Developmental Disabilities, 1050 Forest Hill Road, 10314, Staten Island, NY, USA aut Lassmann H. Institute for Brain Research, Austrian Academy of Sciences, Vienna, Austria aut Iqbal K. New York State Institute for Basic Research in Developmental Disabilities, 1050 Forest Hill Road, 10314, Staten Island, NY, USA aut Joshi J. Department of Biochemistry, University of Tennessee, 37996-0840, Knoxville, TN, USA aut Acta Neuropathologica Springer-Verlag 81/2(1990-12-01), 105-110 0001-6322 81:2<105 1990 81 401 https://doi.org/10.1007/BF00334497 text/html Onlinezugriff via DOI 1 research-article jats NATIONALLICENCE 856 40 https://doi.org/10.1007/BF00334497 text/html Onlinezugriff via DOI NATIONALLICENCE 700 1- Grundke-Iqbal I. New York State Institute for Basic Research in Developmental Disabilities, 1050 Forest Hill Road, 10314, Staten Island, NY, USA aut NATIONALLICENCE 700 1- Fleming J. Department of Biochemistry, University of Tennessee, 37996-0840, Knoxville, TN, USA aut NATIONALLICENCE 700 1- Tung Y. New York State Institute for Basic Research in Developmental Disabilities, 1050 Forest Hill Road, 10314, Staten Island, NY, USA aut NATIONALLICENCE 700 1- Lassmann H. Institute for Brain Research, Austrian Academy of Sciences, Vienna, Austria aut NATIONALLICENCE 700 1- Iqbal K. New York State Institute for Basic Research in Developmental Disabilities, 1050 Forest Hill Road, 10314, Staten Island, NY, USA aut NATIONALLICENCE 700 1- Joshi J. Department of Biochemistry, University of Tennessee, 37996-0840, Knoxville, TN, USA aut NATIONALLICENCE 773 0- Acta Neuropathologica Springer-Verlag 81/2(1990-12-01), 105-110 0001-6322 81:2<105 1990 81 401 Metadata rights reserved Springer special CC-BY-NC licence nationallicence BK010053 XK010053 XK010000 NATIONALLICENCE NATIONALLICENCE NL-springer