Abstracts

Alzheimer disease (AD), an important cause of dementia, generally not associated to epilepsy, is characterized by entorhinal cortex neuronal degeneration and consequent loss of innervation of the [italic]fascia dentata (FD)[/italic]. Mesial temporal lobe epilepsy (MTLE) with hippocampal sclerosis generally presents abnormal mossy fiber sprouting in the inner molecular layer of the FD. The main goal of this work was to study neuron density and mossy fiber distribution in the hippocampus of patients with AD and to compare them to those observed in MTLE patients in order to check if the innervation loss of the FD is always associated to abnormal mossy fiber sprouting. Hippocampal histological sections from AD patients without epilepsy (n=7), surgically treated MTLE patients (n=8) and autopsy controls (n=7 and 8 , respectively) were studied for granule cell, hilar, CA4, CA3, CA2, CA1 and subiculum neuron densities and semiquantitative immunoreactivity to dynorphin as a marker of mossy fibers. Results showed the following: 1) compared to autopsies, AD patients showed a similar neuron densities in all evaluated areas; 2) in contrast, compared to autopsies, MTLE patients showed less granular cells (176427[plusmn] 20465 and 313854[plusmn] 26705) and CA1 (9953[plusmn] 1925 and 24390[plusmn] 956), CA2 (8567[plusmn] 1545 and 22421[plusmn] 1605), CA3 (7328[plusmn] 1236 and 21875[plusmn] 1826) and CA4 (7000[plusmn] 1237 and 17937[plusmn] 1005) pyramidal cells/cubic millimeter; 3) compared to autopsies, AD patients presented a similar distribution of dynorphin immunoreactivity in the outer and inner molecular, granular layer and hilus of the [italic]FD[/italic] as well in CA4; 4) MLTE patients presented higher dynorphin immunoreactivity in the inner molecular layer of the [italic]FD[/italic] than their autopsy controls (gray level 136[plusmn] 4 and 116,6[plusmn] 1, respectively). Data indicate that the loss of human [italic]FD[/italic] innervation is not necessarily associated with mossy fiber sprouting in contrast with results observed in rats with induced unilateral entorhinal lesions and experimental models of MTLE. (Supported by CNPq and FAPESP)