Accumulation of apolipoprotein E and β-amyloid-like protein in a trace of the hippocampal CA1 pyramidal cell layer after ischaemic delayed neuronal death

Ishimaru, Hirohisa; Ishikawa, Ken; Haga, Shukoh; Shoji, Mikio; Ohe, Yuichiro; Haga, Chie; Sasaki, Atsushi; Takashashi, A; Maruyama, Yūji

doi:10.1097/00001756-199611250-00054

Cited by 44 publications

(52 citation statements)

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“…[1][2][3][4][5][6]27,28 Immunocytochemical analysis revealed heavy staining of ␤APP epitopes at both the amino and the carboxyl ends of the molecule in large round cells, most probably macrophages derived from the blood and/or brain. A␤ immunostaining was more prominent in penumbral reactive astrocytes and especially in small spherical structures of older rats as compared with young rats, suggesting that the aged brain presents relatively favorable conditions for the focal accumulation of A␤.…”

Section: Discussionmentioning

confidence: 99%

“…2 In rodents, ␤APP expression is increased in the brain after cerebral ischemia, [3][4][5] and there is evidence for the accumulation of A␤ as well. 6 Kalaria et al 3 showed that at 4 and 7 days postocclusion, ␤APP immunoreactivity is preferentially localized within axonal swellings, dystrophic neurites, and neuronal perikarya along the periphery of the infarct.…”

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confidence: 99%

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β-Amyloid Precursor Protein and β-Amyloid Peptide Immunoreactivity in the Rat Brain After Middle Cerebral Artery Occlusion

Popa‐Wagner

Schröder

Walker

et al. 1998

Stroke

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Background and Purpose-Previous studies have shown that the ␤-amyloid precursor protein (␤APP) is upregulated after cerebral ischemia and that the ␤-amyloid (A␤) fragment may be toxic to brain cells. Although stroke in humans usually afflicts the elderly, most experimental studies on the nature of cerebral ischemia have used young animals. To test the hypothesis that the upregulation and/or persistence of amyloidogenic proteins is exacerbated in aged rats after cerebral ischemic stroke, we studied the expression of ␤APP and its proteolytic product A␤ in the brains of young and old rats 7 days after temporary cerebral ischemia. Methods-Focal cerebral ischemia was produced by reversible occlusion of the right middle cerebral artery in 3-and 20-month-old male Sprague-Dawley rats. After 1 week, brains were removed and immunostaining was performed for ␤APP, A␤, and ED1 for macrophages and glial fibrillary acidic protein (GFAP). Results-Histological staining revealed that the degree of necrotic cavitation in the infarct core was relatively less in aged rats than in young rats, suggesting a slower pace of degenerative change and/or tissue removal in older animals. ␤APP immunoreactivity was robustly increased, primarily in macrophage-like, ED1-positive cells in the infarct core and in the penumbra of both young and aged animals. A␤ immunoreactivity was evident in GFAP-positive astrocytic somata and processes, and also in clusters of small spherical structures in the penumbra. These A␤-immunoreactive minispheres were more numerous in aged rats than in young rats. Conclusions-The presence of ␤APP and A␤ immunoreactivity in the infarct core and penumbra indicates that cerebral ischemia promotes conditions that are favorable to the focal accumulation of ␤APP and its proteolytic fragments, especially in the aged brain. (Stroke. 1998;29:2196-2202.)

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

β-Amyloid Precursor Protein and β-Amyloid Peptide Immunoreactivity in the Rat Brain After Middle Cerebral Artery Occlusion

Popa‐Wagner

Schröder

Walker

et al. 1998

Stroke

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“…Animals after focal and global ischemic brain injury with a survival time up to 1 year presented increased brain immunoreactivity to the -amyloid peptide and as well as to the N-and C-terminal of amyloid precursor protein. The staining was observed extracellularly and intracellularly (Pluta et al, 1994b;Hall et al, 1995;Tomimoto et al, 1995;Horsburgh, Nicoll, 1996a;Ishimaru et al, 1996a;Yokota et al, 1996;Pluta et al, 1997b;Pluta et al, 1998b;Lin et al, 1999;Pluta 2000;Lin et al, 2001;Sinigaglia-Coimbra et al, 2002;Fujioka et al, 2003;. Different fragments of amyloid precursor protein were noted in astrocytes, neurons, oligodendrocytes, and microglia (Banati et al, 1995;Palacios et al, 1995;Pluta et al, 1997b;Nihashi et al, 2001;Pluta, 2002a;Pluta2002b;Badan et al, 2003;Badan et al, 2004).…”

Section: Amyloid Precursor Protein and β-Amyloid Peptide After Ischemiamentioning

confidence: 97%

“…Extracellular accumulations of apolipoproteins were irregular and well delineated and mainly diffuse. 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).…”

Section: Apolipoproteins After Ischemiamentioning

confidence: 99%

“…intechopen.com aforementioned observations indicate that the late neurotoxic -amyloid peptide and C-terminal of amyloid precursor protein deposition after ischemic brain injury may represent a secondary injury process that could deteriorate the ischemic brain outcome by unexpected additional neurons death (Pluta et al, 1997c, Pluta et al, 1998b. Following ischemia -amyloid peptide is produced as a result of neurons injury (Ishimaru et al, 1996a) and probably appears its effects, influencing ischemic neurons and glia as dementia. It is generally received that -amyloid peptide takes part in neurons death (Cotter et al, 1999).…”

Section: Amyloid Precursor Protein and β-Amyloid Peptide After Ischemiamentioning

confidence: 99%

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Alzheimer's Factors in Ischemic Brain Injury

Pluta¹,

Jabłoński²

2012

Brain Injury - Pathogenesis, Monitoring, Recovery and Management

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Alzheimer's Mechanisms in Ischemic Brain Degeneration

Pluta

Ułamek

Jabłoński³

2009

The Anatomical Record

108

293

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There is increasing evidence for influence of Alzheimer's proteins and neuropathology on ischemic brain injury. This review investigates the relationships between b-amyloid peptide, apolipoproteins, presenilins, tau protein, a-synuclein, inflammation factors, and neuronal survival/ death decisions in brain following ischemic episode. The interactions of these molecules and influence on b-amyloid peptide synthesis and contribution to ischemic brain degeneration and finally to dementia are reviewed. Generation and deposition of b-amyloid peptide and tau protein pathology are important key players involved in mechanisms in ischemic neurodegeneration as well as in Alzheimer's disease. Current evidence suggests that inflammatory process represents next component, which significantly contribute to degeneration progression. Although inflammation was initially thought to arise secondary to ischemic neurodegeneration, recent studies present that inflammatory mediators may stimulate amyloid precursor protein metabolism by upregulation of b-secretase and therefore are able to establish a vicious cycle. Functional brain recovery after ischemic lesion was delayed and incomplete by an injuryrelated increase in the amount of the neurotoxic C-terminal of amyloid precursor protein and b-amyloid peptide. Moreover, ischemic neurodegeneration is strongly accelerated with aging, too. New therapeutic alternatives targeting these proteins and repairing related neuronal changes are under development for the treatment of ischemic brain consequences including memory loss prevention.

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Accumulation of apolipoprotein E and β-amyloid-like protein in a trace of the hippocampal CA1 pyramidal cell layer after ischaemic delayed neuronal death

Cited by 44 publications

References 0 publications

β-Amyloid Precursor Protein and β-Amyloid Peptide Immunoreactivity in the Rat Brain After Middle Cerebral Artery Occlusion

β-Amyloid Precursor Protein and β-Amyloid Peptide Immunoreactivity in the Rat Brain After Middle Cerebral Artery Occlusion

Alzheimer's Factors in Ischemic Brain Injury

Alzheimer's Mechanisms in Ischemic Brain Degeneration

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