Section 3 Aging and Dementia

**91**

**Chapter 5**

**Abstract**

Approach

*Stavros J. Baloyannis*

Treatment, cerebrum, cerebellum

humanitarian consequences.

**1. Introduction**

Mitochondria in the Cerebral and

Cerebellar Cortex in Alzheimer's

Disease, Target for a Therapeutic

Alzheimer's disease remains the main cause of dementia in advanced age worldwide. Among the etiopathological background of the disease mitochondrial alterations may play a crucial role, given that they are closely related to metabolic and energy deficiency in neurons, glia, and endothelial cells in Alzheimer's disease and other neurodegenerative disorders. In a series of morphological and morphometric studies of mitochondria in the cerebrum and the cerebellar cortex in Alzheimer's disease, by electron microscopy, we described marked morphological and morphometric alterations. The most frequent ultrastructural alterations of the mitochondria consist of disruption of the cristae, accumulation of osmiophilic material, and marked changes of shape and size in comparison with the normal controls. Mitochondrial alterations were particularly prominent in dendritic profiles and dendritic spines. The ultrastructural study of a substantial number of neurons in the cerebellum revealed that mitochondrial alterations do not coexist, as a rule, with the typical Alzheimer's pathology, such as cytoskeletal alterations, amyloid deposits, and tau pathology, though they are frequently observed coexisting with alterations of the cisternae of the Golgi apparatus. Therapeutical regimes targeting

mitochondria may be beneficial in early cases of Alzheimer's disease.

**Keywords:** Alzheimer's disease, Mitochondria, Electron microscopy, Oxidative stress

Alzheimer's disease is the main causative factor of presenile and senile dementia [1] involving a large number of potential pathogenetic mechanisms, which for years was extinguishing the mental capacities, affecting seriously the cognition of the patients and leading to a tragic epilogue of the life with many social, economic and

The phenomenology of familial or sporadic Alzheimer's disease is the final act of a drama, which gradually was causing selective and progressive neuronal loss [2], extensive synaptic alterations [3, 4], progressive neurofibrillary degeneration [5] resulting in intracellular accumulation of hyperphosphorylated tau protein [6], in the form of neurofibrillary tangles, with a parallel accumulation of extracellular

## **Chapter 5**
