Literature DB >> 8321160

Neuritic plaques in Alzheimer disease originate from neurofibrillary tangles.

G Perry1.   

Abstract

Amyloid beta-protein is a major focus in efforts to understand the etiology of Alzheimer disease yet there is little known about the mechanism of its deposition in plaques. I propose deposition of amyloid in neuritic plaques depends on the remains of neurofibrillary tangles after neuronal death. The interaction of these two lesions means neuritic plaques are not only dependent on neurofibrillary tangles and neuronal death but also dependent on their concurrence.

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Year:  1993        PMID: 8321160     DOI: 10.1016/0306-9877(93)90051-q

Source DB:  PubMed          Journal:  Med Hypotheses        ISSN: 0306-9877            Impact factor:   1.538


  3 in total

1.  Distribution of granulocyte-monocyte colony-stimulating factor and its receptor α-subunit in the adult human brain with specific reference to Alzheimer's disease.

Authors:  Sami Ridwan; Henrike Bauer; Katrin Frauenknecht; Harald von Pein; Clemens J Sommer
Journal:  J Neural Transm (Vienna)       Date:  2012-03-20       Impact factor: 3.575

2.  Immunocytochemical evidence that the beta-protein precursor is an integral component of neurofibrillary tangles of Alzheimer's disease.

Authors:  G Perry; P L Richey; S L Siedlak; M A Smith; P Mulvihill; D A DeWitt; J Barnett; B D Greenberg; R N Kalaria
Journal:  Am J Pathol       Date:  1993-12       Impact factor: 4.307

3.  The spatial patterns of beta/A4 deposit subtypes in Down's syndrome.

Authors:  R A Amstrong
Journal:  Acta Neuropathol       Date:  1994       Impact factor: 17.088

  3 in total

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