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STZ-induced diabetic rats) may not exhibit the advanced structural changes and fiber loss seen in human neuropathy [11]

These researchers further demonstrated that this synaptic dysfunction was caused by these human A42 dimeric oligomers by completely blocking the disruption of synaptic plasticity by passive immunization with antibodies to A42 dimers

Finally, the combined therapy reduced the relapse rate from 43.7% to 10.5% and more than doubled its latency, from an average of 3 weeks to an average of 7 weeks

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Acetylcholine, in particular, is highly vulnerable to this neuroinflammatory state

Lavie CJ, Church TS, Milani RV, Earnest CP