ABSTRACT
An in-depth understanding of the anatomy of the craniocervical junction (CCJ) is indispensable in skull base neurosurgery. In this paper, we discuss the osteology of the occipital bone, the atlas (C1) and axis (C2), the ligaments and the muscle anatomy of the CCJ region and their relationships with the vertebral artery. We will also discuss the trajectory of the vertebral artery and review the anatomy of the jugular foramen and lower cranial nerves (IX to XII). The most important surgical approaches to the CCJ, including the far lateral approach, the anterolateral approach of Bernard George and the endoscopic endonasal approach, will be discussed to review the surgical anatomy.
Subject(s)
Cervical Atlas , Occipital Bone , Skull Base , Humans , Skull Base/anatomy & histology , Skull Base/surgery , Cervical Atlas/anatomy & histology , Cervical Atlas/surgery , Occipital Bone/anatomy & histology , Occipital Bone/surgery , Atlanto-Occipital Joint/anatomy & histology , Atlanto-Occipital Joint/surgery , Vertebral Artery/anatomy & histology , Neurosurgical Procedures/methods , Cervical Vertebrae/anatomy & histology , Cervical Vertebrae/surgery , Atlanto-Axial Joint/anatomy & histology , Atlanto-Axial Joint/surgery , Cranial Nerves/anatomy & histology , Axis, Cervical Vertebra/anatomy & histology , Axis, Cervical Vertebra/surgeryABSTRACT
Synapse loss occurs early and correlates with cognitive decline in Alzheimer's disease (AD). Synaptotoxicity is driven, at least in part, by amyloid-beta oligomers (Aßo), but the exact synaptic components targeted by Aßo remain to be identified. We here tested the hypotheses that the post-synaptic protein Neuroligin-1 (NLGN1) is affected early in the process of neurodegeneration in the hippocampus, and specifically by Aßo, and that it can modulate Aßo toxicity. We found that hippocampal NLGN1 was decreased in patients with AD in comparison to patients with mild cognitive impairment and control subjects. Female 3xTg-AD mice also showed a decreased NLGN1 level in the hippocampus at an early age (i.e., 4 months). We observed that chronic hippocampal Aßo injections initially increased the expression of one specific Nlgn1 transcript, which was followed by a clear decrease. Lastly, the absence of NLGN1 decreased neuronal counts in the dentate gyrus, which was not the case in wild-type animals, and worsens impairment in spatial learning following chronic hippocampal Aßo injections. Our findings support that NLGN1 is impacted early during neurodegenerative processes, and that Aßo contributes to this effect. Moreover, our results suggest that the presence of NLGN1 favors the cognitive prognosis during Aßo-driven neurodegeneration.
