DLB
The results suggest that: 1) IGF-I, IGF-II, and neurotrophin signaling are more impaired in DLB than PD, corresponding with DLB's more pronounced neurodegeneration, oxidative stress, and alpha-synuclein accumulation; 2) MnCl2 exposure causes PD/DLB associated abnormalities in central nervous system neurons, and therefore may contribute to their molecular pathogenesis; and 3) molecular abnormalities in PD/DLB overlap with but are distinguishable from Alzheimer's disease.
The results suggest that: 1) IGF-I, <span class="gene" id="19276553-6-36-42">IGF-II</span>, and neurotrophin signaling are more impaired in <span class="disease" id="19276553-6-92-95">DLB</span> than PD, corresponding with <span class="disease" id="19276553-6-124-127">DLB</span>'s more pronounced neurodegeneration, oxidative stress, and alpha-synuclein accumulation; 2) MnCl2 exposure causes PD/<span class="disease" id="19276553-6-245-248">DLB</span> associated abnormalities in central nervous system neurons, and therefore may contribute to their molecular pathogenesis; and 3) molecular abnormalities in PD/<span class="disease" id="19276553-6-408-411">DLB</span> overlap with but are distinguishable from Alzheimer's disease.