The Acoustic Cortex in Frontal Dementia

What is it about?

Frontal dementia is a clinical entity of cognitive impairment, characterized mostly by progressive loss of  uency in speech, eventually resulting in aphasia or anomia, associated frequently with early loss of insight and many forms of inappropriate behavior. Hyperphosphorylation of the isoforms of tau protein, a microtubule-associated protein, which plays an important role in the pathogenetic mechanisms of Alzheimer’s disease, is mainly involved in the pathogenesis of frontal dementia. In the present study, the morphological alterations of the acoustic cortex are described in three cases of dementia who fulŽ lled all the clinical and neuropathological criteria of frontal dementia. Specimens from the acoustic area of the temporal cortex were processed with Golgi silver impregnation techniques, Cajal and Rio Hortega stainings and electron microscopy. A tremendous loss of Cajal-Retzius neurons in layer I of the acoustic cortex was noticed in Golgi staining, associated with dense reactive astrocytosis, visualized clearly in Cajal gold impregnation technique. Loss of dendritic spines was extensively seen in layers III, V, and VI in correlation with normal controls. The electron microscopy revealed numerous Pick bodies, whose tau protein was the main protein constituent. Paired helical Ž laments were seen in the perikaryon and the axons of the neurons of layers IV, V, and VI. Synaptic alterations were extensively seen in the acoustic cortex consisting mainly of degeneration of the postsynaptic components. The authors think that the impressive morphological alterations of the acoustic cortex in frontal dementia might explain the early onset of deŽ ciency of communication that most of the patients demonstrate in the initial stage of the disease.

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Why is it important?

An impressive decrease of neuronal population was observed under the light microscope in all the cases of frontal dementia in comparison with normal controls. The Cajal–Retzius cell, a very functional neuron of layer I of the acoustic cortex , was impressively reduced in number, and had been replaced by numerous reactive astrocytes in many places of Hessl gyri . Astrocytosis is also obvious in layers II, III, V, and VI; very well visualized in Cajal staining.A marked reduction of the dendritic Ž elds of the neurons was also noticed in all the layers of the acoustic cortex. The majority of the neurons lacked the tertiary dendritic branches and demonstrated a substantial abbreviation of dendritic arborization. A tremendous loss of dendritic spines was noticed in all the specimens in comparison with normal controls. In electron microscopy, Pick bodies were seen in the cytoplasm of numerous neurons of layers II, III, V, and VI. Swollen chromatolytic neurons were also diffusely seen in all the layers of the acoustic cortex. Paired helical Ž laments (PHF) were seen in the perikaryon and the axons of the neurons of layers IV, V, and VI. The neuronal synapses were diminished compared with normal controls. Most of the synapses demonstrated a marked polymorphism of the presynaptic vesicles and pronounced thickness of the postsynaptic membrane.

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