By inserting correcting genes into the brain of monkeys, scientists produce sustained low levels of a protein, called GDNF, that induces neuroprotection and behavioral recovery in experimental PD.
On the basis of data collected in over 2900 patients, information useful for the differential diagnosis between PD and other parkinsonisms is provided.
PD patients who thought they had received a transplant of neural cells in their brains - but who really had not - reported an improved quality of life one year later.
These substances are able to dissolve fibrillar and amorphous deposits of both amiloid and synuclein proteins associated respectively with Alzheimer's and Parkinson's diseases.
Physical anhedonia is a relatively frequent, although mild, affective disturbance of PD, independent from neurological, frontal and depressive aspects.
This finding goes against the hypothesis that there is a “pre-parkinsonian” personality that avoids the consumption of substances that induce dependence
Protection against nigral cell degeneration using either a calpain inhibitor, or through the overexpression of calpastatin, an endogenous antagonist, significantly restores locomotor activity in experimental PD.
Aging and PD may be associated with a reduction in the capacity to eliminate the hydrocarbon n-hexane, a solvent possibly involved in the pathogenesis of PD.