The cause, or causes, of the vast majority of Alzheimer's disease cases are unknown. A number of contributing factors have been postulated, including infection. It has long been known that the spirochete Treponema pallidum, which is the infective agent for syphilis, can in its late stages cause dementia, chronic inflammation, cortical atrophy and amyloid deposition. Spirochetes of unidentified types and strains have previously been observed in the blood, CSF and brain of 14 AD patients tested and absent in 13 controls. In three of these AD cases spirochetes were grown in a medium selective for Borrelia burgdorferi.In the present study, the phylogenetic analysis of these spirochetes was made. Positive identification of the agent as Borrelia burgdorferi sensu stricto was based on genetic and molecular analyses. Borrelia antigens and genes were co-localized with beta-amyloid deposits in these AD cases. The data indicate that Borrelia burgdorferi may persist in the brain and be associated with amyloid plaques in AD. They suggest that these spirochetes, perhaps in an analogous fashion to Treponema pallidum, may contribute to dementia, cortical atrophy and amyloid deposition. Further in vitro and in vivo studies may bring more insight into the potential role of spirochetes in AD.

The site of formation of C-reactive protein (CxRP, CRP) has been studied with tissues from rabbits, monkeys, and human beings. Rabbits and monkeys were stimulated to produce the acute phase protein by injection of turpentine, croton oil, endotoxin, paratyphoid-typhoid vaccine, or pneumococci. C14-amino acid incorporation in vitro was demonstrated by means of autoradiography of immunoelectrophoretic patterns made with culture fluids. It was found that among many different tissues tested liver was the only tissue which incorporated C14-lysine and isoleucine into CxRP or CRP. Only livers taken 16 to 24 hr after various stimuli were active; livers from normal animals or from animals killed 3 to 9 hr after stimulation did not produce detectable amounts of CxRP. Inflamed muscle from the injection site did not show C14-amino acid incorporation into CxRP. Several human tissues were also cultured, and a few liver cultures found to contain labeled CRP. The formation of CxRP or CRP by the liver was always accompanied by enhanced C14-amino acid incorporation into other serum proteins, but the reverse was not always found.

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The phenotype of 165 gastrointestinal stromal tumours was studied by immunohistochemistry. In each case the phenotype was compared to the histological diagnosis. The phenotype was muscle in 49 tumours (30%), neural in 18 (11%), histiocytic in 20 (12%) and mixed in five (3%); 68 tumours (41%) were positive for vimentin only, four tumours had no markers and one tumour was positive for keratin only. Histologically, the tumours were classified as smooth muscle, probably smooth muscle, probably nerve sheath tumours or tumours of undetermined differentiation. In 30 histologically unequivocal muscle tumours, the phenotype was muscle in 28. Half of them, all benign, arose in the oesophagus or gastric cardia. Apart from this group, there was no correlation between phenotype, site of tumour and histological differentiation. Actin was a more sensitive muscle marker than desmin. With the exception of oesophageal tumours, the histological appearances alone could not establish a diagnosis of malignancy and were inadequate in evaluating differentiation. Immunohistochemical examination determined differentiation in 54% of the tumours, but this finding should be interpreted with caution in terms of histogenesis. It allowed us, however, to specify the differential diagnosis in 57 tumours in which the histological diagnosis was uncertain.

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