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Altered expression of genes for amyloid and cytoskeletal proteins in alzheimer cortex
Author(s) -
Clark Arthur W.,
Krekoski Craig A.,
Parhad Irma M.,
Liston Dane,
Julien JeanPierre,
Hoar David I.
Publication year - 1989
Publication title -
annals of neurology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.764
H-Index - 296
eISSN - 1531-8249
pISSN - 0364-5134
DOI - 10.1002/ana.410250404
Subject(s) - glial fibrillary acidic protein , biology , cytoskeleton , neurofilament , messenger rna , cortex (anatomy) , cerebral cortex , alzheimer's disease , amyloid precursor protein , tau protein , microbiology and biotechnology , gene expression , intermediate filament , amyloid (mycology) , neurodegeneration , gene , neuroscience , pathology , immunology , biochemistry , cell , medicine , immunohistochemistry , disease , botany
Recent studies have indicated a normal gene dose for the amyloid precursor protein (APP) in Alzheimer's disease (AD). These findings leave open the possibility that elevated levels of messenger RNA (mRNA) for this protein may contribute to the pathogenesis of AD. Using Northern analysis, we compared the levels of mRNA for the APP and 3 cytoskeletal proteins in parietal cortex of 6 brains having marked AD‐type degeneration with the levels of these mRNAs in 6 control samples. The cytoskeletal mRNAs studied were those for the human neurofilament 68‐kDa subunit (HNFL), for α‐tubulin, and for glial fibrillary acidic protein (GFAP). A ribonuclease (RNase) protection assay was also used to compare AD and control HNFL mRNA levels. The mRNAs for APP, HNFL, and α‐tubulin were diminished in AD cortex. The decrement for APP mRNA was less than that for HNFL or α‐tubulin. The message for GFAP in AD cortex showed no loss. The findings support a general deficit in neuronal mRNAs, including that for APP. They do not exclude the possibility of elevated levels of the message for the APP in small neuronal subsets, in subcortical neurons projecting to cortex, or as a generalized phenomenon in earlier stages of the disease.