ABSTRACT
The upper end of the central canal of the human spinal cord has been repeatedly implicated in the pathogenesis of various diseases, yet its precise normal position in the medulla oblongata and upper cervical spinal cord remains unclear. The purpose of this study is to describe the anatomy of the upper end of the central canal with quantitative measurements and a three-dimensional (3D) model. Seven formalin-embalmed human brainstems were included, and the central canal was identified in serial axial histological sections using epithelial membrane antigen antibody staining. Measurements included the distances between the central canal (CC) and the anterior medullary fissure (AMF) and the posterior medullary sulcus (PMS). The surface and perimeter of the CC and the spinal cord were calculated, and its anterior-posterior and maximum lateral lengths were measured for 3D modeling. The upper end of the CC was identified in six specimens, extending from the apertura canalis centralis (ACC) to its final position in the cervical cord. Positioned on the midline, it reaches its final location approximately 15 mm below the obex. No specimen showed canal dilatation, focal stenosis, or evidence of syringomyelia. At 21 mm under the ACC in the cervical cord, the median distance from the CC to the AMF was 3.14 (2.54-3.15) mm and from the CC to the PMS was 5.19 (4.52-5.43) mm, with a progressive shift from the posterior limit to the anterior third of the cervical spinal cord. The median area of the CC was consistently less than 0.1 mm2. The upper end of the CC originates at the ACC, in the posterior part of the MO, and reaches its normal position in the anterior third of the cervical spinal cord less than 2 cm below the obex. Establishing the normal position of the upper end of this canal is crucial for understanding its possible involvement in cranio-cervical junction pathologies.
ABSTRACT
The neuropathological changes of limbic-predominant age-related TDP-43 encephalopathy (LATE) are frequent in the aged population and are now recognized as a cause of memory impairment. However, it remains unknown if this proteinopathy is also present in other primate species. We thus investigated the presence and distribution of TDP-43 pathology in the hippocampus and amygdala of 7 aged memory-impaired rhesus macaques (Macaca mulatta, 18-32 years old) from 2 different cohorts. While present in an FTLD-TDP case used as a positive control for immunostaining, we found no TDP-43 or phosphorylated TDP-43 immunoreactive neuronal cytoplasmic inclusion in the amygdala or the hippocampus of these aged animals (as well as in young and mature macaques used as negative controls). We concluded that LATE is probably a human-specific condition, such as many other proteinopathies, and does not participate in age-related memory impairment in non-human primates.
