Complete cerebral ischemia with short-term survival in rat induced by cardiac arrest. II. Extracellular and intracellular accumulation of apolipoproteins E and J in the brain

Original article Laminar distribution of β-amyloid (Aβ) peptide deposits in the frontal lobe in familial and sporadic Alzheimer’s disease

“…Laminar distributions of Aβ deposits in frontal lobe AD are essentially similar in the FAD and SAD cases examined and similar whether Apo E allele ε4 was present or not [31]. In addition, among FAD cases, there was no evidence that a specific type of laminar distribution was influenced by genetic subtype.…”

Alzheimer's Factors in Ischemic Brain Injury

“…Diffuse, broad, but faint areas were also seen. Extracellular apolipoproteins E and J staining were strongly labeled by antibody to apolipoprotein A1, stronger than by apolipoprotein E antibody (Kida et al, 1995;Pluta et al, 1995a). They were immunostained stronger by antibody to apolipoprotein E than apolipoprotein J (Kida et al, 1995;Pluta et al, 1995a).…”

“…Strong staining was noted also in acellular, necrotic, irregular and spiderlike foci (Kida et al, 1995;Pluta et al, 1995a;Ishimaru et al, 1996a). It is important to notice that accumulations of apolipoproteins colocalize with aggregates of different parts of amyloid precursor protein (Kida et al, 1995;Pluta et al, 1995b). Apolipoprotein E promotes the deposition of -amyloid peptide into the oligomeric and the fibrillar form.…”

“…-amyloid peptide 42 can be moved by the blood-brain barrier receptor mediated system (Deane et al, 2003;Deane et al, 2004a;Deane et al, 2004b) and by blood-brain barrier leakage caused by ischemic brain injury (Pluta et al, 1996;Pluta et al, 1997a;Pluta et al, 1999;Pluta et al, 2000) or -amyloid peptide toxicity on blood-brain barrier after ischemia (Thomas et al, 1996;Fiala et al, 1998;Farkas et al, 2003;Paris et al, 2004a;Paris et al, 2004b). The pathological immunostaining for apolipoproteins A1, E and J was observed mainly around vessels (Kida et al, 1995;Pluta 2000). Perivascular deposits of above proteins were well delineated and irregular.…”

“…Moreover, pathological overexpression of clusterin suggests that the synthesis of this protein was a result of selective delayed neuronal death rather than involvement in the pathological cascade of events that cause it (Walton et al, 1996). The pathological immunostaining for apolipoproteins A1, E, and J was shown extracellularly and intracellularly (Hall et al, 1995;Kida et al, 1995;Pluta et al, 1995a;Horsburgh, Nicoll 1996a, Horsburgh, Nicoll 1996bIshimaru et al, 1996b;Pluta 2000;Kamada et al, 2003). Intracellular staining was noted in damaged neurons exhibiting features of ischemic injury (Pluta 2000).…”