Treatment of Alzheimer's Disease with Anti-Homocysteic acid Antibody

Homocysteic acid (HA) may play an important role in Alzhiemer disease (AD) as we previously reported that HA induced accumulation of intraneuronal A[beta]42. In this study, we first analyzed HA levels in a mouse model of AD. 4-month old pre-pathologic 3xTg-AD mice exhibited higher levels of HA in the hippocampus as compared to age-matched nontransgenic, suggesting that HA accumulation may precede both A[beta] and tau pathologies. To further determine the pathogenic role of HA in AD, we treated young 3xTg-AD mice with vitamin B6-deficient food for 3 weeks to induce the production of HA in the brain. Concominantly, mice received either saline or anti-HA antibody intraventricularly using a guide cannula every 3 days. Mice received anti-HA antibody significantly rescued cognitive impairment induced by vitamin B6 deficiency. Pathologically, 3-week treatment with vitamin B-6 deficient food resulted in strong neurodegeneration in the hippocampal CA1 zone and decreased hippocampal volume. In contrast, anti-HA antibody treatment attenuated these pathological changes. Taken together, we conclude that increased brain HA triggers memory impairment whose condition was deteriorated by amyloid and subsequent neurodegeneration and reduction of neurogenesis. Our results indicate a pathogenic role of HA in AD

Treatment of Alzheimer's Disease with Anti-Homocysteic acid Antibody

Homocysteic acid (HA) may play an important role in Alzhiemer disease (AD) as we previously reported that HA induced accumulation of intraneuronal A[beta]42. In this study, we first analyzed HA levels in a mouse model of AD. 4-month old pre-pathologic 3xTg-AD mice exhibited higher levels of HA in the hippocampus as compared to age-matched nontransgenic, suggesting that HA accumulation may precede both A[beta] and tau pathologies. To further determine the pathogenic role of HA in AD, we treated young 3xTg-AD mice with vitamin B6-deficient food for 3 weeks to induce the production of HA in the brain. Concominantly, mice received either saline or anti-HA antibody intraventricularly using a guide cannula every 3 days. Mice received anti-HA antibody significantly rescued cognitive impairment induced by vitamin B6 deficiency. Pathologically, 3-week treatment with vitamin B-6 deficient food resulted in strong neurodegeneration in the hippocampal CA1 zone and decreased hippocampal volume. In contrast, anti-HA antibody treatment attenuated these pathological changes. Taken together, we conclude that increased brain HA triggers memory impairment whose condition was deteriorated by amyloid and subsequent neurodegeneration and reduction of neurogenesis. Our results indicate a pathogenic role of HA in AD

From Risk Communication to Participatory Radiation Risk Assessment

In the aftermath of the Fukushima nuclear accident, many of the post-disaster responses undertaken by the Japanese government sparked vivid debates and criticisms from the civil society. These concern emergency responses such as the revision of public exposure dose limit, designation of evacuation zones, distribution of iodine tablets, and risk communication as well as mid and long-term policies including radiation dose monitoring, decontamination, waste management, return of evacuees, and health and food monitoring. Convinced that such public agitation derived from their lack of scientific knowledge, the authorities undertook a strategy to enhance their communication on radiological risk and its health effects. In this paper, we attempt to challenge the traditional notion of “risk communication” which considers that the concerned risks have been clearly defined by the scientific community and that the problem simply remains in communicating them “rightly” to the population. We argue, in contrary, that risks cannot be properly defined without understanding the “real” concern of the population – what they consider as risks - nor taking into account existing scientific controversies and uncertainties. In such a context, what we need is not so much of risk communication but rather participatory risk assessment where risks are debated by multiple stakeholders and actors including counter- or independent experts and third parties such as NPOs, and are defined collectively rather than decided single-handedly by policymakers – the authorities and their affiliated experts. The paper is drawn from the preliminary results of the SHINRAI (‘trust’ in Japanese) project led by the French Institute for Radiological Protection and Nuclear Safety (IRSN), in collaboration with Sciences Po Paris and Tokyo Institute of Technology (Tokyo Tech). This research examines the relation between science, expertise, trust and decisions in the aftermath of the Fukushima nuclear accident by conducting an extensive field interviews in the affected areas of the Fukushima prefecture

B6 deficient feeding or homocysteic acid induces the earlier Alzheimer's pathological change in normal C57BL male mice

It is the first report that the earlier Alzheimer's pathological changes can be induced in normal C57BL mice, by B6 deficient feeding for 3 month, and this pathological changes were completely inhibited by anti-homocysteic acid antibody. According to Koch's postulate, if a pathogen of Alzheimer's disease is administrated to the normal animal, we would observe the Alzheimer's pathology in the normal animal. We actually have observed this pathology in normal C57BL male mice

Bismuth-Based Visible-Light-Active Photocatalytic Nanomaterials for Environmental Remediation

Bismuth-based semiconductors are regarded as a promising new candidate of advanced photocatalytic nanomaterials due to their suitable optical band gap energy for visible light absorption, an increased mobility of photogenerated charge carriers because of well-dispersed Bi 6s orbital, non-toxicity, and easy tailoring of their morphologies owing to their layered structure

Treatment of Alzheimer's Disease with Anti-Homocysteic Acid Antibody in 3xTg-AD Male Mice

Alzheimer's disease (AD) is an age-associated progressive neurodegenerative disorder with dementia, the exact pathogenic mechanisms of which remain unknown. We previously reported that homocysteic acid (HA) may be one of the pathological biomarkers in the brain with AD and that the increased levels of HA may induce the accumulation of intraneuronal amyloid-beta (Aβ) peptides. In this study, we further investigated the pathological role of HA in a mouse model of AD. Four-month-old prepathological 3xTg-AD mice exhibited higher levels of HA in the hippocampus than did age-matched nontransgenic mice, suggesting that HA accumulation may precede both Aβ and tau pathologies. We then fed 3-month-old 3xTg-AD mice with vitamin B6-deficient food for 3 weeks to increase the HA levels in the brain. Concomitantly, mice received either saline or anti-HA antibody intraventricularly via a guide cannula every 3 days during the course of the B6-deficient diet. We found that mice that received anti-HA antibody significantly resisted cognitive impairment induced by vitamin B6 deficiency and that AD-related pathological changes in their brains was attenuated compared with the saline-injected control group. A similar neuroprotective effect was observed in 12-month-old 3xTg-AD mice that received anti-HA antibody injections while receiving the regular diet. We conclude that increased brain HA triggers memory impairment and that this condition deteriorates with amyloid and leads to subsequent neurodegeneration in mouse models of AD

Cardiac Sarcoidosis Culminating in Severe Biventricular Failure

A 59-year-old woman with a history of lung sarcoidosis developed general edema and exertional dyspnea. An electrocardiogram showed first-degree atrioventricular block with complete right bundle branch block. Chest X-ray showed cardiomegaly. Echocardiography showed diffuse and severe hypokinesis of the left ventricle (LV) and biventricular enlargement with severe tricuspid regurgitation. Myocardial scintigraphy disclosed a perfusion defect at the ventricular septum and hypoperfusion at the posterior wall and the apex. On cardiac catheterization, pulmonary capillary wedge pressure, right ventricular, and right atrial pressures were elevated. Coronary angiograms were normal. Myocardial biopsy of the right ventricle histologically revealed epithelioid cell granuloma with infiltration of fibrous cells. The patient's symptom and LV function were improved with conventional medical therapy for heart failure. This is a rare case of cardiac sarcoidosis resulting in biventricular failure