Mitochondrial Alterations in Peripheral Mononuclear Blood Cells from Alzheimer’s Disease and Mild Cognitive Impairment Patients

• Published in: Oxidative medicine and cellular longevity 2016-01, Vol.2016 (2016), p.1-11
• Main Authors: Lanni, C., Memo, M., Uberti, D., Cuetos, F., Novelli, A., Arce Varas, N., Buizza, L., Marziano, M., Prandelli, C., Abate, G., Delbarba, A., Martinez, C.
• Format: Article
• Language: English
• Subjects: Advertising executives; Aged; Aged, 80 and over; Alzheimer Disease - blood; Alzheimer's disease; Biosynthesis; Blood; Blood platelets; Case-Control Studies; Cell Nucleus - metabolism; Cognitive ability; Cognitive Dysfunction - blood; Cytochrome b; Cytochrome c; Cytochromes b - metabolism; Cytochromes c - metabolism; DNA, Mitochondrial - metabolism; Enzymes; Female; Gene Dosage; Gene expression; Genetic transcription; Genomes; Hospitals; Humans; Leukocytes, Mononuclear - cytology; Lymphocytes; Male; Middle Aged; Mitochondria - metabolism; Mitochondria - pathology; Mitochondrial DNA; Oxidants - metabolism; Oxidation-Reduction; Oxidative stress; Pathology; Proteins; Real-Time Polymerase Chain Reaction; RNA polymerase; Studies; Superoxide Dismutase - metabolism; Transcription factors
• ISSN: 1942-0900; 1942-0994
• DOI: 10.1155/2016/5923938

It is well recognized that mitochondrial dysfunction contributes to neurodegeneration occurring in Alzheimer’s disease (AD). However, evidences of mitochondrial defects in AD peripheral cells are still inconclusive. Here, some mitochondrial-encoded and nuclear-encoded proteins, involved in maintaining the correct mitochondria machine, were investigated in terms of protein expression and enzymatic activity in peripheral blood mononuclear cells (PBMCs) isolated from AD and Mild Cognitive Impairment (MCI) patients and healthy subjects. In addition mitochondrial DNA copy number was measured by real time PCR. We found some differences and some similarities between AD and MCI patients when compared with healthy subjects. For example, cytochrome C and cytochrome B were decreased in AD, while MCI showed only a statistical reduction of cytochrome C. On the other hand, both AD and MCI blood cells exhibited highly nitrated MnSOD, index of a prooxidant environment inside the mitochondria. TFAM, a regulator of mitochondrial genome replication and transcription, was decreased in both AD and MCI patients’ blood cells. Moreover also the mitochondrial DNA amount was reduced in PBMCs from both patient groups. In conclusion these data confirmed peripheral mitochondria impairment in AD and demonstrated that TFAM and mtDNA amount reduction could be two features of early events occurring in AD pathogenesis.