Mitochondrial dysfunctions are significant contributors to neurodegeneration. One result or a cause of mitochondrial dysfunction might be the disruption of mtDNA transcription. Limited data indicated an altered expression of mtDNA encoded transcripts in Alzheimer's disease (AD) or Parkinson's disease (PD). The number of mitochondria is high in cells with a high energy demand, such as muscle or nerve cells. AD or PD involves increased risk of cardiomyopathy, suggesting that mitochondrial dysfunction might be systemic. If it is systemic, we should observe it in different cell types. Given that, we wanted to investigate any disruption in the regulation of mtDNA encoded gene expression in addition to PINK1, PARKIN, and ATP levels in peripheral blood samples of PD cases who are affected by a neurodegenerative disorder that is very well known by its mitochondrial aspects. Our results showed for the first time that: 1) age of onset > 50 PD sporadic (PDS) cases: mtDNA transcription and quality control genes were affected; 2) age of onset <50 PDS cases: only mtDNA transcription was affected; and 3) PD cases with familial background: only quality control genes were affected. mtDNA

Background Alzheimer's Disease (AD) is a progressive complex neurodegenerative disorder clinical characterized by demolishing cognitive functions and behavioral abilities. Until recently, molecular mechanisms of AD have not been clarified yet. Alterations in biochemical and molecular pathways in patients suffering from AD may not only emerge in the brain but also could affect blood cells and vessels. Platelets are the blood cells that have a crucial function in the regulation of hemostasis and also play an important role in pathophysiological conditions such as neurodegenerative diseases, including AD.Methods In the current study, analyzed platelet function by optical density in 43 AD patients and 45 controls. White-Matter changes evaluated by MRI Axial FLAIR images (Fazekas scale). We measured the serum levels of vWF and GP1b proteins by ELISA and hsa-miR-26a-5p and hsa-mir24-3p by qRT-PCR analysis.Results ADP-induced platelet aggregation decreased in AD (p = 0.016). We evaluated aspirin (ASA) usage and detected that AD patients free of ASA have a significantly higher platelet function. Serum GP1b levels are a significant increase in AD (p = 0.018). The relative expression levels of hsa-miR-26a-5p are significantly low in AD (p = 0.001). A positive significant correlation was found between the relative expression values of hsa-miR-24-3p and hsa-miR-26a-5p in both control groups and AD ( p = 0.0051, r = 0.4149, 95% CI = 0.1256–0.6392; p = 0.0023, r = 0.6820, 95% CI 0.4728–0.8184)Conclusion The present study implicates that increased expression of serum GP1b and decreased relative expression levels of hsa-miR-26a-5p in AD. As a conclusion, we suggest that GP1b and hsa-miR-26a-5p essential roles of platelet function in AD.

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