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Amyloid beta-protein 1-42 (Abeta42) is believed to play a causative role in the development of Alzheimer disease (AD), although it is a minor part of Abeta. In contrast, Abeta40 is the predominant secreted form of Abeta and recent studies have suggested that Abeta40 has neuroprotective effects and inhibits amyloid deposition. We have reported that(More)
Proteins having relations to hereditary dwarfism of the rdw rat (gene symbol: rdw) were searched for in various tissues of the rat with an improved two-dimensional gel electrophoresis technique followed by immunoblotting and microsequencing. Tissues inspected were cerebral cortex, cerebellum, brain trunk, hypothalamus, pituitary, thyroid gland, liver,(More)
Angiotensin II receptor blockers (ARBs) are widely prescribed for the medication of systemic hypertension and congestive heart failure. It has been reported that ARBs can reduce the risk for the onset of Alzheimer's disease (AD) and have beneficial effects on dementia. Neurotoxic amyloid β-protein (Aβ) is believed to play a causative role in the development(More)
The longer and neurotoxic species of amyloid-β protein (Aβ), Aβ42 and Aβ43, contribute to Aβ accumulation in Alzheimer's disease (AD) pathogenesis and are considered to be the primary cause of the disease. In contrast, the predominant secreted form of Aβ, Aβ40, inhibits amyloid deposition and may have neuroprotective effects. We have reported that(More)
BACKGROUND Conduction system defects and slowed ventricular conduction are common in patients with systolic dysfunction and contribute to arrhythmias and sudden death. In animal models of heart failure, cardiac alpha1-adrenergic signaling is constitutively activated. Here, we report the effects of constitutive activation of alpha1-adrenergic signaling on(More)
Melanie Meyer-Luehmann et al. recently reported that amyloid plaques form extremely rapidly-within one day, in three mouse models of Alzheimer's disease studied longitudinally in vivo [1]. However, the 'rapid appearance' of 'newborn' amyloid plaques can also be the result of delayed visualization of existing amyloid plaques, which is caused by the increase(More)
Alzheimer's disease is characterized by neuronal loss and cerebral accumulation of amyloid-β protein (Aβ) and lowering the generation of Aβ is a pivotal approach in the strategy of Alzheimer's disease treatment. Midlife hypertension is a major risk factor for the future onset of sporadic Alzheimer's disease and the use of some antihypertensive drugs may(More)
The cerebral microcapillary endothelium, known as the blood-brain barrier (BBB), acts as a barrier between the blood and the interstitial fluid of the brain. The BBB therefore controls the passage of nutrients into the central nervous system (CNS). Microglia show a specific affinity for migration into the CNS, and this migration appears to occur(More)
A longer amyloid-β protein (Aβ), Aβ43, deposits in amyloid plaques more frequently than Aβ40 in both sporadic and familial Alzheimer's disease (AD) brains, which shares a similar feature of Aβ42 [1,2]. A recent study reported that Aβ43 is more amyloidogenic and neurotoxic than Aβ42 in vitro and is abundant in the brain of patients with Alzheimer's disease(More)
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