Although TH, AAD and GAD were significantly decreased in the cortex of treated animals, the reduction was not correlated with the development of the electroclinical patterns of epilepsy.
We describe the inherited folate sensitive fragile site, fra(2)(q13), in three unrelated mentally retarded children, two of them with different forms of epilepsy.
Here, we report the mapping of an epilepsy gene to a specific chromosomal region, on the basis of cosegregation of two closely-linked DNA markers with a form of epilepsy known as benign familial neonatal convulsions (BFNC2, 12120 in ref.3).
Although SGP-2 transcripts, and hence pTB16, were recently shown to be increased in neurodegenerative diseases such as scrapie in hamsters and Alzheimer disease in humans, our observations with brain tumors and epilepsy are suggestive of a role for pTB16 in neuropathologies in general and support the hypothesis of its involvement in tissue remodeling and cell death.
HYP in combination with MEL enhanced synergistically SCEs and cell division delays in both groups with synergistic effects in cells from epileptics (P less than 0.01 and P less than 0.01 respectively) higher than from controls (P less than 0.05 and P less than 0.05 respectively.
These data suggest that BDNF and its receptor may play a local role within the hippocampus in kindling-associated neural plasticity and in neuronal protection following epileptic, ischemic, and hypoglycemic insults.
In studies starting from a neurobiological genetic point of view including the whole spectrum of PPR, the phenomenon could be shown to be a widespread condition being only loosely associated with epilepsy, but more often with symptoms of psychovegetative instability.