[Automobile driving among patients with dementia. Survey in the Poitou-Charentes region].

Objectives: To determine the characteristics of drivers with dementia and analyze their driving habits.

Methods: The study was conducted among neurologists and geriatricians in the Poitou-Charentes region. We asked 75 physicians to question (according to a structured questionnaire) the patients they saw in January 2004 who were known to suffer from dementia, defined by a Folstein Mini-Mental State (MMS) score pound 25.

mTOR/p70S6k signalling alteration by Abeta exposure as well as in APP-PS1 transgenic models and in patients with Alzheimer's disease.

In Alzheimer's disease, neuropathological hallmarks include the accumulation of beta-amyloid peptides (Abeta) in senile plaques, phosphorylated tau in neurofibrillary tangles and neuronal death. Abeta is the major aetiological agent according to the amyloid cascade hypothesis. Translational control includes phosphorylation of the kinases mammalian target of rapamycin (mTOR) and p70S6k which modulate cell growth, proliferation and autophagy.

The up-regulation of the striatal dopamine transporter's activity by cAMP is PKA-, CaMK II- and phosphatase-dependent.

The neuronal dopamine transporter (DAT) is a presynaptic plasma membrane protein mediating the re-uptake of dopamine released from synaptic cleft into the nerve terminals. While the regulation of its activity by protein kinase C signalling is well-characterized, there is controversial debate about its regulation by protein kinase A (PKA) signalling. In rat striatal synaptosomes, we showed that a cell-permeable cyclic adenosine 3',5'-monophosphate analogue up-regulated the DAT capacity without modification of its efficiency.

Lactic acidosis progressively impairs dopamine uptake in rat striatal synaptosomes by a mechanism partially independent of the Na+/K+-ATPase dysfunction.

Previous experiments reported that incubation of rat striatal synaptosomes with lactic acid (pH 5.5) resulted in an inhibition of dopamine (DA) uptake partially mediated by free radical damage. Since the DA uptake process is highly dependent on the functionality of Na+/K+-ATPase, the present study investigated whether this inhibition of DA uptake could be related to an alteration of the Na+/K+-ATPase activity.