**4. Conclusions**

AD mouse models [173]. These findings suggest that these subcellular structures are affected

**Figure 3. Mitochondrial impairment as a potential biomarker for early diagnosis of AD**. Diagram shows that possi‐ ble markers of mitochondrial damage could be present in blood plasma, blood cells and skin fibroblasts from AD pa‐ tients. The compressive evaluation of mitochondrial health in these tissues could early detect neurodegenerative

Interestingly, a recent study with fibroblasts from an AD patient demonstrated that is possible to induce the differentiation of dermal fibroblasts into neuronal cells [174]. This study demonstrated that those neurons derived from fibroblasts expressed significant levels of phosphorylated tau and presented significant changes in the expression of genes associated with AD [174]. These studies indicate that the fibroblasts of patients could be a reliable tool for obtaining physiological information that reflects the neurological state of the patients.

Peripheral biomarkers with effective action in the early detection of Alzheimer's pathology are currently unknown, but the evidence of possible markers of mitochondrial damage in blood plasma, blood cells and skin fibroblasts represents an important step in the search for an AD biomarker (**Figure 3**). Although the fact that these tissues may provide less invasive and inexpensive sources to investigate AD progression, the finding of a new biomarker would not only be important for early diagnosis but also be an opportunity to prove direct and person‐ alized therapies in patients with AD. Future research should focus not only in search for therapies of the disease but also in the search for a good and safe model to test the effectiveness

changes reported in AD.

362 Update on Dementia

of these pathways proposed.

in AD and this would not be considered an isolated effect of fibroblasts culture.

The focus of this chapter is to discuss the principal pathways involved in mitochondrial dysfunction seen in different models of AD. We present clear evidence that showed defects in mitochondrial morphology, bioenergetics and mitochondrial axonal transport, and how these alterations lead to an impaired neuronal communication in AD. Also, we discussed different therapeutic that reduce mitochondrial damage in AD. It is important to say that several of these therapies had probe to improve not only mitochondrial health but also the neuropatho‐ logical damage in AD. Finally, we showed that those mitochondrial alterations are also present in several peripheral tissues. This is a relevant aspect to consider because it could represent a promising diagnostic method, and also an easy and accessible tool for measuring the progres‐ sion and development of AD.
