Deposition of PrP amyloid in cerebral vessels in conjunction with neurofibrillary lesions is the neuropathologic hallmark of the dementia associated with a stop mutation at codon 145 ofPRNP, the gene encoding the prion protein (PrP). In this disorder, the vascular amyloid in tissue sections and the -7.5-kDa fragment extracted from amyloid are labeled by antibodies to epitopes located in the PrP sequence including amino acids 90-147. Amyloid-laden vessels are also labeled by antibodies against the C terminus, suggesting that PrP from the normal allele is involved in the pathologic process. Abundant neurofibrillary lesions are present in the cerebral gray matter. They are composed of paired helical filaments, are labeled with antibodies that recognize multiple phosphorylation sites in T protein, and are similar to those observed in Alzheimer disease. A PrP cerebral amyloid angiopathy has not been reported in diseases caused by PRNP mutations or in human transmissible spongiform encephalopathies; we propose to name this phenotype PrP cerebral amyloid angiopathy (PrP-CAA).

Aim:The aim of this study was to clinically evaluate percutaneous endoscopic gastrostomy (PEG) tube feeding of elderly Japanese patients with dementia.Method: The records of the 155 patients with dementia who underwent PEG in Juntendo Tokyo Koto Geriatric Medical Center were reviewed for pertinent clinical data, including diagnosis of dementia, place of stay before and after hospitalization, as well as survival rate, albumin levels, and incidence of aspiration pneumonia (AP) before and 6 months after PEG feeding. The latter three data of these patients were compared with those of 106 patients with dementia fed through a nasogastric (NG) tube.

No abstract

No abstract

I-FP-CIT SPECT may play a role for detecting DLB among the subjects in prodromal stage. During this stage, long-term olfactory dysfunction and/or RBD may indicate more severe degeneration of the nigro-striatal dopaminergic pathway.