INCREASED NEURONAL BETA-AMYLOID PRECURSOR PROTEIN EXPRESSION IN HUMANTEMPORAL-LOBE EPILEPSY - ASSOCIATION WITH INTERLEUKIN-1-ALPHA IMMUNOREACTIVITY

Levels of immunoreactive beta-amyloid precursor protein and interleuki n-1 alpha were found to be elevated in surgically resected human tempo ral lobe tissue from patients with intractable epilepsy compared with postmortem tissue from neurologically unaffected patients (controls). In tissue from epileptics, the levels of the 135-kDa beta-amyloid prec ursor protein isoform were elevated to fourfold (p < 0.05) those of co ntrols and those of the 130-kDa isoform to threefold (p < 0.05), where as those of the 120-kDa isoform (p > 0.05) were not different from con trol values. beta-Amyloid precursor protein-immunoreactive neurons wer e 16 times more numerous, and their cytoplasm and proximal processes w ere more intensely immunoreactive in tissue sections from epileptics t han controls (133 +/- 12 vs. 8 +/- 3/mm(2); p < 0.001). However, neith er beta-amyloid precursor protein-immunoreactive dystrophic neurites n or beta-amyloid deposits were found in this tissue. Interleukin-1 alph a-immunoreactive cells (microglia) were three times more numerous in e pileptics than in controls (80 +/- 8 vs. 25 +/- 5/mm(2); p < 0.001), a nd these cells were often found adjacent to beta-amyloid precursor pro tein-immunoreactive neuronal cell bodies. Our findings, together with functions established in vitro for interleukin-1, suggest that increas ed expression of this protein contributes to the increased levels of b eta-amyloid precursor protein in epileptics, thus indicating a potenti al role for both of these proteins in the neuronal dysfunctions, e.g., hyperexcitability, characteristic of epilepsy.