Sk. Singhrao et al., NEW IMMUNOCYTOCHEMICAL EVIDENCE FOR A NEURONAL OLIGODENDROGLIAL ORIGIN FOR CORPORA-AMYLACEA/, Neuropathology and applied neurobiology, 20(1), 1994, pp. 66-73
Studies employing a bank of antisera applied to sections of LR White e
mbedded AD and normal ageing brain tissue, may throw new light on the
derivation of CA. Conspicuous levels of immunoreactivity were found in
the CA of both tissues with markers for oligodendrocytic proteins suc
h as antisera against myelin basic proteolipid protein, galactocerebro
side and myelin/oligodendrocyte glycoprotein. CA were unreactive with
MRC OX-42, a marker for microglia and macrophages. In a previous publi
cation [22] we demonstrated that the much more abundant CA in the brai
ns of Alzheimer's disease (AD) sufferers, although slightly more varie
d in their immunoreactivity than those found in normally ageing contro
ls, were universally immunoreactive with anti-tau, a neuronally derive
d protein and often also contained amyloid. The cores of CA were not i
mmunoreactive with anti-GFAP, suggesting a lack of involvement with as
trocytes. Our results now show that in addition to amyloid and neurona
l proteins, a significant proportion of the content of CA is derived f
rom oligodendrocytes and/or myelin. The substantial Fe peak previously
reported [22] following X-ray microanalysis of CA was probably due to
ferritin. However, immunostaining with antisera to ferritin showed th
at high ferritin immunoreactivity was common to both micro- and macrog
lia as well as CA. More significantly, the immunoreactivity of CA with
anti-ubiquitin [22] suggests that degeneration of neuronal/oligodendr
ocytic elements may precede CA formation.