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Brain ischemia and ischemic blood-brain barrier as etiological factors in sporadic Alzheimer's disease.

Pluta R, Amek MU - Neuropsychiatr Dis Treat (2008)

Bottom Line: Chronic disruption of the blood-brain barrier after ischemic injury was shown.As an effect of chronic ischemic blood-brain barrier injury, a visible connection of amyloid plaques with neurovasculature was observed.This neuropathology appears to have similar distribution and mechanisms to Alzheimer's disease.

View Article: PubMed Central - PubMed

Affiliation: Laboratory of Ischemic and Neurodegenerative Brain Research, Department of Neurodegenerative Disorders, Medical Research Centre, Polish Academy of Sciences, Warsaw, Poland.

ABSTRACT
The development of neuronal death and amyloid plaques is a characteristic feature of ischemic- and Alzheimer-type dementia. An important aspect of neuronal loss and amyloid plaques are their topography and neuropathogenesis. This review was performed to present the hypothesis that different fragments of blood-borne amyloid precursor protein are able to enter the ischemic blood-brain barrier. Chronic disruption of the blood-brain barrier after ischemic injury was shown. As an effect of chronic ischemic blood-brain barrier injury, a visible connection of amyloid plaques with neurovasculature was observed. This neuropathology appears to have similar distribution and mechanisms to Alzheimer's disease. The usefulness of rival ischemic theory in elucidating the neuropathogenesis of amyloid plaques formation and neuronal death in Alzheimer's disorder is discussed.

No MeSH data available.


Related in: MedlinePlus

Role of estrogen in ischemic β-amyloid peptide neuropathology and ischemic brain cells injury.Abbreviation: BBB, blood–brain barrier.
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f2-ndt-4-855: Role of estrogen in ischemic β-amyloid peptide neuropathology and ischemic brain cells injury.Abbreviation: BBB, blood–brain barrier.

Mentions: The incidence of Alzheimer’s disease cases is gender-related (Pluta 2006a) and the risk of Alzheimer’s disease in women is significantly greater than in men. The cumulative risk for Alzheimer’s disease in women is greater because of a lack of estrogen (Figure 2) after menopause, which has been proposed as a risk factor for Alzheimer’s disease among women (Pluta 2006a). Estrogen effects have been presented as blood–brain barrier function control through intercellular junction proteins (Kang et al 2006) and/or intracellular transport elements and through protective effects on the cellular components of barrier such as endothelial, pericytes, and astrocytes cells (Yang et al 2005), cells which are vulnerable to aging and ischemia (Table 1) influence in the context of normal blood–brain barrier activity (Figure 2) (Sohrabji 2007; Zipser et al 2007). Pathological permeability of the blood–brain barrier can expose brain parenchyma to different elements of blood (Table 2) that directly and/or indirectly harm neuronal cells (Table 1) and potentate other neuropathological processes. Age-related cascades in different areas of the brain can have far reaching consequences for cognitive ability and affect. Most investigators have taken the approach of studying estrogen influence on neuropathological events related to Alzheimer’s disease (Figure 2) (Simpkins et al 1997; Dubal et al 1998; Shi et al 1998; Chi et al 2002, 2005). Estrogens exert neuroprotective activity in experimental models of brain ischemia (Figure 2) (Simpkins et al 1997; Dubal et al 1998; Shi et al 1998; Chen et al 2001; Chi et al 2002; Yang et al 2005), but the precise mechanism of their protection is not clearly understood. These hormones may preserve neuronal health (Chen et al 2001) by maintaining the integrity of the blood–brain barrier (Figure 2) (Chi et al 2002, 2005). Another possibility is that estrogen attenuates overexpression of amyloid precursor protein messenger RNA (Shi et al 1998). The protective effects of estrogens are seen in all of the neurovascular unit components including vascular endothelial cells, astrocytes, microglia, and neurons (Chen et al 2001; Yang et al 2005). Additionally postischemic estrogens reduce hypoperfusion and secondary ischemic episodes following brain ischemia (McCullough et al 2001). Prevention of brain ischemia and treatment ischemic episodes may have significant implications for Alzheimer’s disease therapy. In view of the earlier observations that cognitive decline is progressing after brain ischemia, there is the distinct possibility that we can prevent this decline by targeting the slowly progressing pathology that follows ischemic injury by aiming at molecular events now shown to change following brain ischemia.


Brain ischemia and ischemic blood-brain barrier as etiological factors in sporadic Alzheimer's disease.

Pluta R, Amek MU - Neuropsychiatr Dis Treat (2008)

Role of estrogen in ischemic β-amyloid peptide neuropathology and ischemic brain cells injury.Abbreviation: BBB, blood–brain barrier.
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC2626921&req=5

f2-ndt-4-855: Role of estrogen in ischemic β-amyloid peptide neuropathology and ischemic brain cells injury.Abbreviation: BBB, blood–brain barrier.
Mentions: The incidence of Alzheimer’s disease cases is gender-related (Pluta 2006a) and the risk of Alzheimer’s disease in women is significantly greater than in men. The cumulative risk for Alzheimer’s disease in women is greater because of a lack of estrogen (Figure 2) after menopause, which has been proposed as a risk factor for Alzheimer’s disease among women (Pluta 2006a). Estrogen effects have been presented as blood–brain barrier function control through intercellular junction proteins (Kang et al 2006) and/or intracellular transport elements and through protective effects on the cellular components of barrier such as endothelial, pericytes, and astrocytes cells (Yang et al 2005), cells which are vulnerable to aging and ischemia (Table 1) influence in the context of normal blood–brain barrier activity (Figure 2) (Sohrabji 2007; Zipser et al 2007). Pathological permeability of the blood–brain barrier can expose brain parenchyma to different elements of blood (Table 2) that directly and/or indirectly harm neuronal cells (Table 1) and potentate other neuropathological processes. Age-related cascades in different areas of the brain can have far reaching consequences for cognitive ability and affect. Most investigators have taken the approach of studying estrogen influence on neuropathological events related to Alzheimer’s disease (Figure 2) (Simpkins et al 1997; Dubal et al 1998; Shi et al 1998; Chi et al 2002, 2005). Estrogens exert neuroprotective activity in experimental models of brain ischemia (Figure 2) (Simpkins et al 1997; Dubal et al 1998; Shi et al 1998; Chen et al 2001; Chi et al 2002; Yang et al 2005), but the precise mechanism of their protection is not clearly understood. These hormones may preserve neuronal health (Chen et al 2001) by maintaining the integrity of the blood–brain barrier (Figure 2) (Chi et al 2002, 2005). Another possibility is that estrogen attenuates overexpression of amyloid precursor protein messenger RNA (Shi et al 1998). The protective effects of estrogens are seen in all of the neurovascular unit components including vascular endothelial cells, astrocytes, microglia, and neurons (Chen et al 2001; Yang et al 2005). Additionally postischemic estrogens reduce hypoperfusion and secondary ischemic episodes following brain ischemia (McCullough et al 2001). Prevention of brain ischemia and treatment ischemic episodes may have significant implications for Alzheimer’s disease therapy. In view of the earlier observations that cognitive decline is progressing after brain ischemia, there is the distinct possibility that we can prevent this decline by targeting the slowly progressing pathology that follows ischemic injury by aiming at molecular events now shown to change following brain ischemia.

Bottom Line: Chronic disruption of the blood-brain barrier after ischemic injury was shown.As an effect of chronic ischemic blood-brain barrier injury, a visible connection of amyloid plaques with neurovasculature was observed.This neuropathology appears to have similar distribution and mechanisms to Alzheimer's disease.

View Article: PubMed Central - PubMed

Affiliation: Laboratory of Ischemic and Neurodegenerative Brain Research, Department of Neurodegenerative Disorders, Medical Research Centre, Polish Academy of Sciences, Warsaw, Poland.

ABSTRACT
The development of neuronal death and amyloid plaques is a characteristic feature of ischemic- and Alzheimer-type dementia. An important aspect of neuronal loss and amyloid plaques are their topography and neuropathogenesis. This review was performed to present the hypothesis that different fragments of blood-borne amyloid precursor protein are able to enter the ischemic blood-brain barrier. Chronic disruption of the blood-brain barrier after ischemic injury was shown. As an effect of chronic ischemic blood-brain barrier injury, a visible connection of amyloid plaques with neurovasculature was observed. This neuropathology appears to have similar distribution and mechanisms to Alzheimer's disease. The usefulness of rival ischemic theory in elucidating the neuropathogenesis of amyloid plaques formation and neuronal death in Alzheimer's disorder is discussed.

No MeSH data available.


Related in: MedlinePlus