Literature DB >> 8096426

Alzheimer's disease-like dystrophic neurites characteristically associated with senile plaques are not found within other neurodegenerative diseases unless amyloid beta-protein deposition is present.

W C Benzing1, E J Mufson, D M Armstrong.   

Abstract

Swollen, bulbous-shaped (dystrophic) neurites are a common pathologic feature of Alzheimer's disease (AD) and represent one of the most abundant neuritic abnormalities within the brains of patients with this disease. In the present study, we sought to determine whether the dystrophic neurites which are observed in association with senile plaques are unique to AD or whether they are characteristic of a more generalized process of neuritic and/or neuronal degeneration which can be observed in other neurodegenerative diseases. To accomplish this, we examined post-mortem brain material from patients with AD, Parkinson's disease (PD), Parkinson's disease with associated AD, Parkinson's disease with dementia yet without AD pathology, Huntington's disease (HD), Pick's disease and normal age-matched controls (NC). Using a battery of antibodies to amyloid beta-protein (A beta P), paired-helical filaments (PHF), tyrosine hydroxylase, substance P, neurotensin, and somatostatin we found that immunolabeled dystrophic neurites of the type characteristically observed in AD, were seen only in cases and in brain regions where A beta P deposition was present. More specifically, brain areas known to display severe afferent and/or local degenerative changes such as the caudate and putamen in all three PD groups, the caudate in the HD cases, and the temporal cortex in the HD and Pick's cases were conspicuously free of these swollen neurites unless A beta P deposition was also present.(ABSTRACT TRUNCATED AT 250 WORDS)

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Year:  1993        PMID: 8096426     DOI: 10.1016/0006-8993(93)91563-8

Source DB:  PubMed          Journal:  Brain Res        ISSN: 0006-8993            Impact factor:   3.252


  19 in total

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2.  Prostaglandin J2 promotes O-GlcNAcylation raising APP processing by α- and β-secretases: relevance to Alzheimer's disease.

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Review 5.  Autophagy failure in Alzheimer's disease--locating the primary defect.

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7.  Aberrant activation of focal adhesion proteins mediates fibrillar amyloid beta-induced neuronal dystrophy.

Authors:  Elizabeth A Grace; Jorge Busciglio
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8.  The ubiquitin-proteasome system and the autophagic-lysosomal system in Alzheimer disease.

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9.  Apoptosis is induced by beta-amyloid in cultured central nervous system neurons.

Authors:  D T Loo; A Copani; C J Pike; E R Whittemore; A J Walencewicz; C W Cotman
Journal:  Proc Natl Acad Sci U S A       Date:  1993-09-01       Impact factor: 11.205

10.  Decreased beta-amyloid and increased abnormal Tau deposition in the brain of aged patients with leprosy.

Authors:  D H Chui; T Tabira; S Izumi; G Koya; J Ogata
Journal:  Am J Pathol       Date:  1994-10       Impact factor: 4.307

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