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Amyloid deposition is associated with c‐Jun expression in Alzheimer's disease and amyloid angiopathy
Author(s) -
Ferrer I.,
Seguí J.,
Planas A. M.
Publication year - 1996
Publication title -
neuropathology and applied neurobiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.538
H-Index - 95
eISSN - 1365-2990
pISSN - 0305-1846
DOI - 10.1111/j.1365-2990.1996.tb01130.x
Subject(s) - cerebral amyloid angiopathy , amyloid precursor protein , alzheimer's disease , p3 peptide , pathology , amyloid (mycology) , biochemistry of alzheimer's disease , bace1 as , c jun , senile plaques , medicine , biology , chemistry , disease , dementia , transcription factor , gene , biochemistry
Since the PAD gene (also called promoter of Alzheimer's disease amyloid A4 precursor gene or amyloid β‐protein precursor promoter) has two AP‐1 consensus sequences, and members of the Fos and Jun families are the major components of the transcription factor activator protein‐1 (AP‐1), we have investigated the localization of c‐Fos and c‐Jun immunoreactivity and its relationship to β‐amyloid deposition in the brains of patients with Alzheimer's disease and amyloid angiopathy. c‐Jun, but not c‐Fos, immunoreactivity is observed in the muscular layer of meningeal and cerebral blood vessels with amyloid angiopathy, and in the soma of glial cells and cellular processes of unknown origin surrounding β‐amyloid deposits in the brain. These results show that c‐Jun may participate in the cascade of events leading to increased β‐APP (β‐amyloid precursor protein) production and β‐amyloid deposition in the brains of patients with Alzheimer's disease and amyloid angiopathy.