Abstract
Senile amyloidotic changes of the brain were investigated in 146 consecutive autopsy cases over the age of 49 years (ranging from 50 to 92, with mean 73.3 in years). The subjects had been admitted to the Department of Geriatrics, University of Tokyo Hospital and Harunaso Hospital (Gunma Prefecture) for chiefly physical diseases. The hippocampus and adjacent areas of the left hemisphere were cut into 6μ-thick specimens after formalin fixation and paraffin embedding, to be examined first by thioflavine T fluorescence microscopy (Saeed and Fine), and subsequently by Congo-red polarizing microscopy (Missmahl). Amyloid in the brain, like in other organs, gave unequivocally strong bluish-white fluorescence through ultraviolet (365mμ) or whitish-yellow through blue light (410mμ) after thioflavine T staining, and also produced green birefringence after Congo red staining. The results were confirmed by other classical stains.
Degenerative changes of amyloid nature included: (1) Alzheimer's neurofibrillary changes, (2) central cores of senile plaques, (3) amyloid degeneration of the vessels (amyloid angiopathy), and (4) amyloid infiltration to the perivascular tissues.
Alzheimer's nourofibrillary changes, which were seen in 118 patients (81%), were fully and equally detectable both by fluorescence and polarizing microscopy. They gave entirely the same optic qualities as other amyloidotic changes, despite some controversies on their amyloid nature based on electron-microscopic observations.
Various forms of senile plaques including so-called primitive plaques were easily detected by fluorescence microscopy because coronas as well as central cores produced some degree of fluorescence. Although amyloid usually existed only in the cores, there were exceptionally two types of senile plaques containing amyloid in other locations, one the plaques with diffuse amyloid deposition also in the coronas, and another the reticular plaques without cores with fiber-or clublike components of amyloid nature. Senile plaques were seen in 58 patients (40%).
Amyloid angipathy occurred in the small vessels in the meningeal space and the outer layer of the cortex, most frequently involving arterioles and precapillaries of 100 to 21μ in diameter in the meningeal space, and precapillaries and capillaries less than 50μ in the cortex. In the capillaries amyloid formed semilunar nodules in the walls, finally obstructing lumens. In the arterioles smooth muscle fibers of the tunica media were more specifically involved, beginning with the smooth muscles immediately beneath the tunica adventitia. In several cases with extensive amyloid angiopathy, larger arteries (500 to 1, 000μ in diameter) and veins were also involved.
Amyloid infiltration to the perivascular tissues, found in only eight patients, was classified into three types. In the first type, plaque-like structures were formed around the central core of amyloid-deposited capillaries. In the second, typical senile plaques occurred adjacent to the small vessels under amyloid degeneration. In the last rare type, there was diffuse and sparse deposition of amyloid around the small arteries with or without amyloid.
