Post-Ischemic Brain Neurodegeneration in the Form of Alzheimer's Disease Proteinopathy: Possible Therapeutic Role of Curcumin.

For thousands of years, mankind has been using plant extracts or plants themselves as medicinal herbs. Currently, there is a great deal of public interest in naturally occurring medicinal substances that are virtually non-toxic, readily available, and have an impact on well-being and health. It has been noted that dietary curcumin is one of the regulators that may positively influence changes in the brain after ischemia. Curcumin is a natural polyphenolic compound with pleiotropic biological properties. The observed death of pyramidal neurons in the CA1 region of the hippocampus and its atrophy are considered to be typical changes for post-ischemic brain neurodegeneration and for Alzheimer's disease. Additionally, it has been shown that one of the potential mechanisms of severe neuronal death is the accumulation of neurotoxic amyloid and dysfunctional tau protein after cerebral ischemia. Post-ischemic studies of human and animal brains have shown the presence of amyloid plaques and neurofibrillary tangles. The significant therapeutic feature of curcumin is that it can affect the aging-related cellular proteins, i.e., amyloid and tau protein, preventing their aggregation and insolubility after ischemia. Curcumin also decreases the neurotoxicity of amyloid and tau protein by affecting their structure. Studies in animal models of cerebral ischemia have shown that curcumin reduces infarct volume, brain edema, blood-brain barrier permeability, apoptosis, neuroinflammation, glutamate neurotoxicity, inhibits autophagy and oxidative stress, and improves neurological and behavioral deficits. The available data suggest that curcumin may be a new therapeutic substance in both regenerative medicine and the treatment of neurodegenerative disorders such as post-ischemic neurodegeneration.

Vitamin B12 deficiency as a cause of severe neurological symptoms in breast fed infant - a case report.

BACKGROUND: Vitamin B12 (cobalamin, cbl) deficiency in children is rare and may occurs in exclusively breast fed infants of mothers on vegetarian or vegan diet with lack of appropriate supplementation. The clinical manifestation of vitamin B12 deficiency include neurological disorders, megaloblastic anemia and failure to thrive. Routine and commonly used laboratory tests such as cell blood count (CBC) or serum vitamin B12 level are sufficient for appropriate diagnosis. Typical therapy is based on intramuscular cobalamin injections. Early diagnosis and early onset of treatment are crucial factors for long-term prognosis of patients as the duration of deficiency may be correlated with the development of long lasting changes in the nervous system. The purpose of this article is to present influence of maternal vitamin B12 deficiency as a cause of infant psychomotor retardation. CASE PRESENTATION: We report the case of a 7 months old girl whose parents sought medical advice due to pathological somnolence and developmental regression of their daughter with onset approximately 2 months prior to the visit. Following several diagnostic tests it was determined that the infant's symptoms were due to vitamin B12 deficiency which was secondary to the mother's latent Addison-Biermer disease. Apart from neurological symptoms the infant also showed megaloblastic anemia which is typical to cobalamin deficiencies. Intramuscular vitamin B12 supplementation resulted in instant improvement of the patient's general condition and blood morphology. Unfortunately, psychological examination indicated long-term psychomotor retardation due to delayed diagnosis of B12 deficiency. CONCLUSIONS: Vitamin B12 levels should be considered during differential diagnosis of neurological symptoms in exclusively breast-fed infants especially if they co-exist with megaloblastic anemia and psychomotor retardation.

The use of recombinant human erythropoietin in the treatment of anaemia of prematurity.

UNLABELLED: Anaemia of prematurity (AOP) is caused by a deficiency of erythropoietin, which stimulates differentiation, and growth of erythroid progenitors. The previous standard of therapy of AOP was erythrocyte transfusions. Following successful clinical trials using recombinant human eryrthropoietin (rHuEpo) to treat adults, the rHuEpo has been used to prevent and treat anaemia in preterm infants. The aim of the study was to evaluate the influence of rHuEpo treatment on parameters of the erythrocytic system in peripheral blood, iron concentration, and unsaturated iron bind capacity (UIBC), as well as on erythrocyte transfusion requirements, in preterm infants with AOP, having no infection and not receiving oxygen support. Twenty-four children with AOP, that were hospitalized during one year, with no signs of infection and without any form of oxygen therapy, were investigated. The rHuEpo was administered subcutaneously 700 U/kg/week, in two doses. Infants: also received oral iron. The percentage of children with AOP treated by supplementary transfusions was compared in two one-year periods, before and after the introduction of rHuEpo therapy. In over 50% of children, satisfactory improvement of erythrocytic picture was achieved after administration of 4-7 doses of rHuEpo. In the year prior to the introduction of rHuEpo therapy, 91% of children with AOP required supplementary red cells transfusions, while only 13% when rHuEpo was applied. CONCLUSIONS: The rHuEpo is the drug of choice in the treatment of anaemia of prematurity. Therapeutic use of rHuEpo markedly diminished quantity of supplementary transfusions in children with AOP.