**Abstract**

Alzheimer's disease is a progressive, irreversible presenile or senile neurodegenerative disorder, implicating mainly the mental faculties, characterized by decline of memory and judgment, learning impairment, loss of professional skills and verbal capacities, alterations of social behavior, decline of motor skills and eventual disarrangement of the autonomic equilibrium. Among the pathogenetic factors, oxidative stress and mitochondrial dysfunction may play an essential role. Alterations of mitochondria may enhance amyloid toxicity, which in turn may aggravate mitochondrial dysfunction. We describe ultrastructural alterations of mitochondria in the soma of neurons, in axons, dendritic profiles and synaptic terminals, in astrocytes in early cases of Alzheimer's disease on various areas of the cerebral and the cerebellar cortex, the hippocampus, the hypothalamus, the mammillary bodies and the medial geniculate body. The morphological and morphometric study of the mitochondria revealed an impressive polymorphism at any area of the brain. The mitochondria demonstrated variation of size and shape, fragmentation of the cristae and marked changes of their structure. The most dramatic mitochondrial alterations were observed in dendritic profiles, spines and synaptic terminals. A substantial number of astrocytes demonstrated mitochondrial alterations, which coexisted with fragmentation of Golgi apparatus and dilatation of the cisternae of the smooth endoplasmic reticulum. On the basis of our observations, we feel that therapeutic strategies aiming at protecting the mitochondria might be beneficial in the treatment of early cases of AD.

**Keywords:** Alzheimer's disease, mitochondria, Golgi apparatus, astrocytes, synapses, electron microscopy
