Colocalization of Aluminum and Iron in Nuclei of Nerve Cells in Brains of Patients with Alzheimer's Disease.

Increasing evidence indicates that metal-induced oxidative stress plays a pivotal role in the pathogenesis of Alzheimer's disease (AD). Recently, the presence of 8-hydroxydeoxyguanosine, a biomarker of oxidative DNA damage, was demonstrated in nuclear DNA (nDNA) in the AD brain. Iron (Fe) is a pro-oxidant metal capable of generating hydroxyl radicals that can oxidize DNA, and aluminum (Al) has been reported to facilitate Fe-mediated oxidation.

Demonstration of aluminum in amyloid fibers in the cores of senile plaques in the brains of patients with Alzheimer's disease.

Aluminum (Al) exposure has been reported to be a risk factor for Alzheimer's disease (senile dementia of Alzheimer type), although the role of Al in the etiology of Alzheimer's disease remains controversial. We examined the presence of Al in the Alzheimer's brain using energy-dispersive X-ray spectroscopy combined with transmission electron microscopy (TEM-EDX). TEM-EDX analysis allows simultaneous imaging of subcellular structures with high spatial resolution and analysis of small quantities of elements contained in the same subcellular structures.

26Al incorporation into the brain of suckling rats through maternal milk.

Aluminium inhibits prenatal and postnatal brain development. However, aluminium incorporation into the brain of sucklings through maternal milk has not yet been well clarified because aluminium lacks a suitable isotope for radioactive tracer experiments. Using 26Al (26AlCl(3)) as a tracer, we measured 26Al incorporation into the brain of suckling rats by accelerator mass spectrometry.

Creutzfeldt-Jakob disease with florid plaques after cadaveric dura mater graft.

A patient with dura-associated Creutzfeldt-Jakob disease (D-CJD) which occurred about 15 years after a dura mater graft is reported in the present study. The prion protein gene analysis disclosed no mutation. The D-CJD was atypical in: (i), the long interval between the onset of ataxia and the occurrence of dementia; (ii), the presence of transient myoclonus; and (iii), the presence of florid plaques in the brain.

Ubiquitin-positive inclusions in ependymal cells.

Ubiquitin-positive inclusions (UbIs) have not been well studied in ependymal cells. Since we detected such UbIs in the central canals of the medulla and spinal cord while investigating UbIs in neurodegenerative diseases, we studied UbIs in the entire ependymal system of 42 patients with various neurological diseases and of 10 non-neurological controls. UbIs were located in the cytoplasm of the ependymal cells, and were round to oval in shape, measuring 4-11 microm in diameter.