Cerebral Accumulation of β-Amyloid Following Ischemic Brain Injury with Long-Term Survival

Alzheimer's Factors in Ischemic Brain Injury

“…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).…”

“…Extracellular accumulation of different fragments of amyloid precursor protein ranged from multifocal widespread very small dots to regular amyloid plaques (Pluta et al, 1994b;Pluta et al, 1998b;Pluta 2000;Pluta 2002b;Pluta 2003). Multifocal and widespread different kinds of amyloid plaques were observed mainly in the ischemic hippocampus, brain and entorhinal cortex, and corpus callosum, and subventriculary (Pluta et al, 1994b;Pluta et al, 1997b;Pluta et al, 1998b;Pluta 2000;Pluta 2003;Pluta 2005;Pluta et al, 2009;Pluta et al, 2010). The accumulation of the -amyloid peptide in astrocytes and the C-terminal of amyloid precursor protein in ischemic neurons underline the likely importance of these two proteins in ischemic brain injury cascade of degeneration (Pluta et al, 1994b;Yokota et al, 1996;Pluta 2002b;Badan et al, 2003;Badan et al, 2004).…”

“…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). Animals with long survival after ischemic brain injury from 0.5 to 1 year showed pathological brain staining only to the -amyloid peptide and to the C-terminal of amyloid precursor protein (Pluta et al, 1998b;Pluta 2000). The reactive astrocytes with deposition of different fragments of amyloid precursor protein might be involved in the development of glial scar (Nihashi et al, 2001;Pluta 2002a;Pluta 2002b;Badan et al, 2003;Badan et al, 2004).…”

“…Probably, this kind of abnormalities is responsible for leukoaraiosis formation after ischemic brain injury . Extracellular accumulation of different fragments of amyloid precursor protein ranged from multifocal widespread very small dots to regular amyloid plaques (Pluta et al, 1994b;Pluta et al, 1998b;Pluta 2000;Pluta 2002b;Pluta 2003). Multifocal and widespread different kinds of amyloid plaques were observed mainly in the ischemic hippocampus, brain and entorhinal cortex, and corpus callosum, and subventriculary (Pluta et al, 1994b;Pluta et al, 1997b;Pluta et al, 1998b;Pluta 2000;Pluta 2003;Pluta 2005;Pluta et al, 2009;Pluta et al, 2010).…”

“…The relationship between brain ischemic injury dementia and Alzheimer's disease type dementia is recently much debated. The mechanisms of the progressive cognitive decline after ischemic brain injury are not yet clear but animal investigations have demonstrated an increase in expression and processing of amyloid precursor protein to -amyloid peptide (Pluta et al, 1994b;Pluta et al, 1997b;Pluta et al, 1997c;Pluta et al, 1998b;Lin et al, 1999;Shi et al, 2000;Lin et al, 2001;Badan et al, 2004;Pluta et al, 2009) and an increase in the phosphorylation of tau protein (Dewar, Dawson 1995;Wen et al, 2004b;Wen et al, 2004c, Wen et al, 2007. Moreover, the common mechanism that links progressive cognitive decline after ischemic brain injury and during Alzheimer's disease is neuroinflammation (Koistinaho et al, 2002), which can cause gradual neurodegeneration during prolonged face of injury.…”