Degenerative axonal changes in the hippocampus and amygdala in Parkinson's disease.

The morphological background of cognitive and emotional impairments in Parkinson's disease (PD) has not yet been fully explained. We evaluated the expression of synaptic proteins: alpha- and beta-synuclein, synaptophysin and synaptobrevin and ultrastructural changes of perikaryons and axons in limbic structures at post-mortem from cases of PD to estimate degenerative axonal pathology in the hippocampus and amygdala [corrected]. Limbic structures (enthorinal cortex, hippocampus, and amygdala) are essential for the cognitive processes and emotional behaviour. We found that presynaptic axon pathology is mostly connected with hippocampal CA2-3 and dentate hilar regions as well as with the cortical and medio-central complexes of amygdala. Heterogeneous immunoreactivity of alpha-synuclein and diversified ultrastructure of Lewy bodies (LBs) and Lewy neurites (LNs) indicate their consecutive developmental stages. We observed an excessive perineuroneal expression of synaptophysin in the dentate hilar region in all PD cases, except one. This suggests that the dysfunction of synapses in this region may result from axonal pathology. Our study indicates a relation between cognitive and behavioural symptomatology in PD and alpha-synuclein dependent axonal pathology in the hippocampus and amygdala.