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In MDCK cells, presenilin-1 (PS1) accumulates at intercellular contacts where it colocalizes with components of the cadherin-based adherens junctions. PS1 fragments form complexes with E-cadherin, beta-catenin, and alpha-catenin, all components of adherens junctions. In confluent MDCK cells, PS1 forms complexes with cell surface E-cadherin; disruption of Ca(2+)-dependent cell-cell contacts reduces surface PS1 and the levels of PS1-E-cadherin complexes. PS1 overexpression in human kidney cells enhances cell-cell adhesion. Together, these data show that PS1 incorporates into the cadherin/catenin adhesion system and regulates cell-cell adhesion. PS1 concentrates at intercellular contacts in epithelial tissue; in brain, it forms complexes with both E- and N-cadherin and concentrates at synaptic adhesions. That PS1 is a constituent of the cadherin/catenin complex makes that complex a potential target for PS1 FAD mutations.

This study was undertaken to identify and quantitate mechanoreceptors in the human anterior cruciate ligament (ACL). Ligaments from six human subjects were obtained at autopsy, cut into cross-sectional segments 1.0-1.5 cm thick, and kept oriented as to the femoral and tibial attachments. The segments were stained in bulk by using a modified gold chloride method, frozen, and sectioned on a sliding microtome at 100 microns. The sections were floated in alcoholic gelatin, mounted on slides, dehydrated, and coverslipped. Serial sections were studied with the light microscope and receptors were photographed. Cross-sectional maps of every tenth section were made outlining the periphery of the ACL and the receptors within that section. With these maps, a computerized, morphometric analysis of the ACL was done, thus obtaining the percentage of receptors in each section and in each ACL. In addition to free nerve endings, two morphologically distinct mechanoreceptors were identified: (1) Ruffini end organs and (2) Pacinian corpuscles. Preliminary morphometric analyses show that populations of mechanoreceptors are greater at the femoral and tibial ends of the ligament and constitute approximately 2.5% of the ligament. Based on these findings the human ACL has the anatomic basis for a discriminating afferent outflow to the central nervous system.

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