Premium
Transferrin receptors in the normal human hippocampus and in Alzheimer's disease
Author(s) -
Morris C. M.,
Candy J. M.,
Kerwin J. M.,
Edwardson J. A.
Publication year - 1994
Publication title -
neuropathology and applied neurobiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.538
H-Index - 95
eISSN - 1365-2990
pISSN - 0305-1846
DOI - 10.1111/j.1365-2990.1994.tb00998.x
Subject(s) - alzheimer's disease , hippocampus , receptor , transferrin receptor , transferrin , neuroscience , disease , medicine , biology , pathology , endocrinology
Several lines of evidence suggest that aluminium may play a role in the pathogenesis of Alzheimer's disease (AD). The iron transport protein transferrin is the major transport protein for aluminium, and aluminium gains access to cells by means of a specific cell surface transferrin receptor. We have assessed the distribution of transferrin receptors in the normal and AD hippocampal formation using [ 3 H]–transferrin ([ 3 H]–Tf) binding and tritium film autoradiography, in order to assess the role of the transferrin receptor in AD. In normal brain, 3 H]–Tf binding was highest in the pyramidal cell layers with CA2> dentate gyrus granule cell layer ≥Cal >CA3 ≥ CA4>subiculum>parahippocampal gyrus. In AD, significant reductions in [ 3 H]–Tf binding were found in CA1, CA2 and CA4 pyramidal cell layers. The reduced [ 3 H]–Tf binding in AD may, however, be due to poor pre–mortem agonal states which correlated with reduced [ 3 H]–Tf binding. The discrepancy between the distribution of transferrin receptors in the hippocampus and those areas which are prone to the formation of senile plaques and neurofibrillary tangles suggests that if transferrin–mediated uptake of aluminium in AD/SDAT is significant in the pathogenesis of this disorder, it is not the only determinant of Alzheimer–type neuropathology.