Alzheimer’s disease (AD) is a neurodegenerative disorder of the brain, inducing
progressive severe presenile and senile cognitive decline, resulting in vegetative stage
eventually. From the etiological point of view the main causative factor, remains unknown,
in spite of the steady augmentation of the research efforts. Golgi staining revealed the
substantial alterations of the dendritic branches and the tremendous loss of spines even in
the initial stages of the disease. Electron microscopy reveals morphological changes of the
mitochondria in neurons and astrocytes associated with fragmentation of cisternae of Golgi
complex and pathological alteration of the dendritic spines, even in areas of the brain,
which demonstrate minimal tau pathology and few amyloid β deposits. It is attempted to
describe the ultrastructural alterations of the cerebellar cortex in early cases of AD,
focusing the study mostly on mitochondria, Golgi apparatus, dendritic branches, dendritic
spines and synapses in the cerebellar hemispheres and the vermis. Mitochondria
demonstrated an impressive polymorphism in the soma, the axonal and dendritic profiles of
Purkinje cells, the climbing fibers, the mossy fibers and the synapses. Electron microscopy
revealed also marked fragmentation of cisternae of Golgi complex in large number of
Purkinje cells, granule and stellate cells in the vermis and the cerebellar hemispheres. The
fragmentation of the Golgi complex and the poverty in vesicles in cis- and trans-Golgi
network in the soma of Purkinje cells in Alzheimer’s brains coincide with the synaptic loss,
the shortage of the dendritic arborization and the pathological alterations of the spines.
Numerous spines included large multivesicular bodies, altered spine apparatus, and unusual
mitochondria. Giant elongated spines were seen in a substantial number of Purkinje cells.
In many presynaptic terminals of parallel and mossy fibers, electron microscopy revealed a
dramatic loss of the synaptic vesicles associated with marked polymorphism. On the basis
of the mitochondrial and Golgi complex pathology, new therapeutic strategies protecting
those organelles might be proposed for the treatment of early cases of AD.
Keywords: Alzheimer’s disease, cerebellum, golgi apparatus, mitochondria,
morphometry, oxidative stress, purkinje cells, ultrastructure.
