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ABSTRACT:Recently ,prion‐like transmission has been found in various amyloidosis .AApoAII amyloid fibrils in mouse senile amyloidosis have exhibited transmissibility .AApoAII amyloid fibrils ,which were excreted from mice and contained in fe‐ces or milk ,cause mouse senile amyloidosis .However ,transmissibility of AApoAII amyloid fibrils through other pathways has not yet been established .In this study ,we injected AApoAII amyloid fibrils into R1 .P1‐A poa2c mice to induce AApoAII sys‐temic amyloidosis .Two months later ,AApoAII amyloid fibrils ,which deposited in the skeletal muscles of amyloid‐affected mice ,were used to induce AApoAII systemic amyloidosis .Mouse senile amyloidosis which deposited in skeletal muscles could induce secondary transmission of AApoAII amyloidosis .The evidence of transmission through skeletal muscles in non‐prion systemic amyloidosis is found in our study .This pathway of transmission provides new insight into the potential for food‐borne pathogenesis and etiology of systemic amyloidosis .
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Objective To study the effects of rehabilitation training on the synaptic ultrastructure of the brain cortex after cerebral ischemia.Methods Sixty rats were randomly divided into a sham operation group,a cerebral ischemia group and a rehabilitation training group.A model of focal cerebral ischemia was created in the rats of the cerebral ischemia and rehabilitation training groups.The rehabilitation training group was given balancing,grasping,rotation and walking training every day.The sham operation group and cerebral ischemia group were kept in normal cages,taking food and moving freely.Electron microscopy was used to observe the density and ultrastructure of the cortical synapses at days 1,7,14 and 21 after the operation.Results In the sham operation group there were numerous synaptic terminals in the cortical neuropil.The majority of synapses were Gray type Ⅱ,containing spherical synaptic vesicles in presynaptic elements.After cerebral ischemia,the number of synaptic terminals had decreased and the synaptic structure was damaged.The synaptic vesicles lessened and dissolved.The presynaptic and postsynaptic membranes became unclear.At 21d after ischemia,the synaptic vesicles had disappeared and the presynaptic and postsynaptic membranes were damaged so seriously that the typical synaptic structure disappeared.After rehabilitation training,the damaged synaptic terminals recovered.Conclusions The synaptic structure was damaged after cerebral ischemia,and the damaged synaptic terminals recovered after rehabilitation training.Rehabilitation training can enhance synaptogenesis in the brain's cortex after cerebral ischemia and promote the recovery of motor function,at least in rats.