Premium
Gallium‐67 as a Potential Marker for Aluminium Transport in Rat Brain: Implications for Alzheimer's Disease
Author(s) -
Pullen R. G. L.,
Candy J. M.,
Morris C. M.,
Taylor G.,
Keith A. B.,
Edwardson J. A.
Publication year - 1990
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.1990.tb08846.x
Subject(s) - transferrin receptor , transferrin , in vivo , blood–brain barrier , encephalopathy , pathogenesis , hippocampus , pathology , chemistry , cerebral cortex , receptor , medicine , central nervous system , endocrinology , biophysics , biology , biochemistry , genetics
Evidence of a link between aluminium and Alzheimer's disease, parkinsonism‐dementia of Guam, and dialysis encephalopathy raises questions regarding the role of this element in the pathogenesis of these conditions. Therefore, we have investigated the use of gallium‐67 ( 67 Ga) as a marker for brain uptake of aluminium. The binding of 67 Ga to plasma proteins has been studied, and the blood‐brain barrier permeability and autoradiographic distribution of this isotope in rat brain determined in vivo. The autoradiographic distribution of 125 I‐Fe‐transferrin receptors in rat brain has also been determined in vitro. Results show that 67 Ga was bound to plasma transferrin, entered the brain with a blood‐brain barrier permeability of 2.48 X 10 ‐6 ml/min/g, and showed a marked regional distribution that was very similar to that of 125 I‐Fe‐transferrin receptors. Our data suggest that the vulnerability of the hippocampus, amygdala, and cerebral cortex in conditions such as those mentioned above may be partly due to an increased uptake and deposition of aluminium in these regions by the iron transport system.