Age-related changes in the brain transfer of blood-borne horseradish peroxidase in the hippocampus of senescence-accelerated mouse

Ueno, Masaki; Akiguchi, Ichiro; Hosokawa, Masanori; Shinnou, Masahiko; Sakamoto, Haruhiko; Takemura, Manabu; Higuchi, Kenichi

doi:10.1007/s004010050609

Cited by 38 publications

(41 citation statements)

References 34 publications

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“…SAMR mice with normal characteristics of aging consist of SAMR1, R2, and R4 strains with a relatively strain-specific pathological phenotype. 23) SAMR1 mice show normal aging process. SAMP8 mice have been reported to accumulate Aβ in the brain, where it forms senile plaques.…”

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confidence: 99%

“…Thus, we quantified the accumulation of Aβ40. A standard peptide and the samples were incubated in microplates coated with the monoclonal antibody BNT77, which recognizes human and rat Aβ (11)(12)(13)(14)(15)(16)(17)(18)(19)(20)(21)(22)(23)(24)(25)(26)(27)(28), for 1 h at 4°C. After washing five times, the plates were incubated with an HRP-conjugated antibody raised against the C-terminus of Aβ40 for 1 h at 4°C.…”

Section: )mentioning

confidence: 99%

“…Alternation rate (%) was calculated as the number of actual alternations performed divided by the number of possible alternations (defined as the number of arm entries minus two) multiplied by 100. [19][20][21][22][23][24][25][26][27][28][29][30] Immunostaining of SAMP8, SAMR1, and Tg2576 mouse brain slices. The remaining brain hemispheres were fixed in 10% formaldehyde and then embedded in paraffin.…”

Section: Spontaneous Alternation In a Y-maze Testmentioning

confidence: 99%

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Aβ induces oxidative stress in senescence-accelerated (SAMP8) mice

Takagane

Nojima

Mitsuhashi

et al. 2015

Bioscience, Biotechnology, and Biochemistry

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According to the amyloid hypothesis, amyloid β accumulates in brains with Alzheimer’s disease (AD) and triggers cell death and memory deficit. Previously, we developed a rice Aβ vaccine expressing Aβ, which reduced brain Aβ levels in the Tg2576 mouse model of familial AD. We used senescence-accelerated SAMP8 mice as a model of sporadic AD and investigated the relationship between Aβ and oxidative stress. Insoluble Aβ and 4-hydroxynonenal (4-HNE) levels tended to be reduced in SAMP8 mice-fed the rice Aβ vaccine. We attempted to clarify the relationship between oxidative stress and Aβ in vitro. Addition of Aβ peptide to the culture medium resulted in an increase in 4-HNE levels in SH-SY5Y cells. Tg2576 mice, which express large amounts of Aβ in their brain, also exhibited increased 4-HNE levels; this increase was inhibited by the Aβ vaccine. These results indicate that Aβ induces oxidative stress in cultured cells and in the mouse brain.

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confidence: 99%

Section: )mentioning

confidence: 99%

Section: Spontaneous Alternation In a Y-maze Testmentioning

confidence: 99%

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Aβ induces oxidative stress in senescence-accelerated (SAMP8) mice

Takagane

Nojima

Mitsuhashi

et al. 2015

Bioscience, Biotechnology, and Biochemistry

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“…28 More bloodborne HRP was transferred in the hippocampus of aged SAMP8 than in the hippocampus of young SAMP8. 31 Ultrastructural examination revealed that uncontrolled passage of HRP in the parajunctional cytoplasm of the endothelial cells was seen in the hippocampus of aged SAMP8, while transendothelial passage of HRP in the basement membrane of vessels in the hippocampus was not found even in aged SAMP8. 29 In addition, ultrastructural features showing BBB damage and immunoreactivity for serum albumin within the basal lamina were seen in the olfactory bulbs of aged SAMP8.…”

Section: Bbb Damage In Experimental Animal Models For Vascular Dementiamentioning

confidence: 99%

Blood‐brain barrier damage in vascular dementia

et al. 2015

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New findings on flow or drainage pathways of brain interstitial fluid and cerebrospinal fluid have been made. The interstitial fluid flow has an effect on the passage of blood-borne substances in the brain parenchyma, especially in areas near blood-brain barrier (BBB)-free regions. Actually, blood-borne substances can be transferred in areas with intact BBB function, such as the hippocampus, the corpus callosum, periventricular areas, and medial portions of the amygdala, presumably through leaky vessels in the subfornical organs or the choroid plexus. Increasing evidence indicates that dysfunction of the BBB function may play a significant role in the pathogenesis of vascular dementia. Accordingly, we have examined which insults seen in patients suffering from vascular dementia have an effect on the BBB using experimental animal models exhibiting some phenotypes of vascular dementia. The BBB in the hippocampus was clearly deteriorated in Mongolian gerbils exposed to acute ischemia followed by reperfusion and also in stroke-prone spontaneously hypertensive rats (SHRSP) showing hypertension. The BBB in the corpus callosum was clearly deteriorated in Wistar rats with permanent ligation of the bilateral common carotid arteries showing chronic hypoperfusion. The BBB in the hippocampus and the olfactory bulb was mildly deteriorated in aged senescence accelerated prone mice (SAMP8) showing cognitive dysfunction. The BBB in the hippocampus was mildly deteriorated in aged animals with hydrocephalus. Mild endothelial damage was seen in hyperglycemic db/db mice. In addition, mRNA expression of osteopontin, matrix metalloproteinase-13 (MMP-13), and CD36 was increased in vessels showing BBB damage in hypertensive SHRSP. As osteopontin, MMP-13 and CD36 are known to be related to brain injury and amyloid β accumulation or clearance, BBB damage followed by increased gene expression of these molecules not only contributes to the pathogenesis of vascular dementia, but also bridges the gap between vascular dementia and Alzheimer's disease.

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“…Thus, earthenware pipe-like subpial medial necrosis and medullary arteriolosclerosis accompanying diffuse white matter lesions in vascular cognitive impairment/Binswanger disease brains appear. 8,9 Moreover, blood-brain barrier alters with aging and even in some normal brain structures such as the olfactory bulb, hippocampus and periventricular areas, [10][11][12] and bloodbrain barrier dysfunctions with the development of capillary collagenosis have been revealed not only in Binswanger disease brains, 13,14 but also spontaneously hypertensive rats and a rat model of chronic cerebral hypoperfusion. 15,16 Recently, it has been shown that the intra-cranial capillary diameter is regulated by pericyte contraction under noradrenergic and purinergic neurotransmitter influences.…”

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Vascular mechanisms of cognitive impairment: roles of hypertension and subsequent small vessel disease under sympathetic influences

Akiguchi

Yamamoto

2009

Hypertens Res

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M ild cognitive impairment (MCI) and vascular cognitive impairment are clinically important in the development of Alzheimer disease (AD) 1 and Binswanger disease/vascular dementia. 2,3 The vascular mechanisms of MCI/vascular cognitive impairment, as well as AD with vascular factors, are likely chronic cerebral ischemia due to both hypertensive lipohyalinotic small artery disease and arteriolar-capillary fibrohyalinosis with subsequent dysfunction of the blood-brain barrier. 4,5 These may ultimately cause multiple lacunes in the basal ganglia and the white matter, as well as white matter rarefaction by alteration in the glia and axons. 4 Sympathetic nerve terminals exist not only in the innermost part of the adventitia, but also in the outer layer of the tunica media in human cerebral arteries. 6 Furthermore, the density of sympathetic terminals in cerebral arterial walls makes up over 30% of the total nerve terminals. 7 These may have roles in the development of angionecrosis/medial necrosis under excessive neurogenic control to smooth muscle layers by repeated arterial constrictions, while maintaining autoregulation of perfusion pressure under persistent hypertension. Thus, earthenware pipe-like subpial medial necrosis and medullary arteriolosclerosis accompanying diffuse white matter lesions in vascular cognitive impairment/Binswanger disease brains appear. 8,9 Moreover, blood-brain barrier alters with aging and even in some normal brain structures such as the olfactory bulb, hippocampus and periventricular areas, 10-12 and bloodbrain barrier dysfunctions with the development of capillary collagenosis have been revealed not only in Binswanger disease brains, 13,14 but also spontaneously hypertensive rats and a rat model of chronic cerebral hypoperfusion. 15,16 Recently, it has been shown that the intra-cranial capillary diameter is regulated by pericyte contraction under noradrenergic and purinergic neurotransmitter influences. 17 All the above findings suggest that a failure in autonomic control of cerebral circulation and damage in blood-brain barrier under untreated hypertension have significant roles in the pathogenesis of MCI/vascular cognitive impairment.The relationship, however, between hypertension and cognitive impairment has long been debated and still remains controversial. The majority of studies suggest that elevated blood pressure (BP) is associated with cognitive decline. 18 Longitudinal studies examining midlife hypertension have reported BP as a risk factor for dementia, suggesting its association with late-life atherosclerosis and vascular mechanisms of dementia. The Honolulu-Asia Aging Study-which tracked 2505 men, ages ranging from 71 to 93 years old, who were dementia-free over a mean of 5.1 years-demonstrated that dementia was significantly associated with high systolic BP, but not with pulse pressure. 19 Hypertension may be expected to predispose patients to the development of small vessel diseases, such as silent lacunar infarcts or white matter lesions, leading to cognitive impairmen...

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Age-related changes in the brain transfer of blood-borne horseradish peroxidase in the hippocampus of senescence-accelerated mouse

Cited by 38 publications

References 34 publications

Aβ induces oxidative stress in senescence-accelerated (SAMP8) mice

Aβ induces oxidative stress in senescence-accelerated (SAMP8) mice

Blood‐brain barrier damage in vascular dementia

Vascular mechanisms of cognitive impairment: roles of hypertension and subsequent small vessel disease under sympathetic influences

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