From a recent study cited by Olsen in the past few days. This study compared TH levels between Incidental Lewy Body Disease and PD.

Neuron density was higher in the ILBD patients than in 13 patients with clinical PD, but the percentage of neurons that were negative for tyrosine hydroxylase (TH), indicating dopaminergic cell dysfunction, was also higher.

[I]The researchers - John Duda (Philadelphia Veterans Affairs Medical Center, Pennsylvania, USA) and colleagues - suggest that these TH-negative cells may be "struggling to survive" in patients with ILBD, but have died in patients with PD, accounting for the low overall neuron density in PD patients (66.7% lower than in patients without Lewy bodies).

Neuronal density in ILBD patients declined in line with increasing burden of α-synuclein, but the proportion of TH-negative cells was not associated with α-synuclein burden, which "further suggests that [Lewy pathology] is not the only cause of nigral neuron loss," comments the team.

Schulz-Schaeffer says: "We should disengage from the notion of Lewy body-associated cell death as the main phenomenon in PD and concentrate on synaptic pathology and axonal degeneration of still-existing cells in our search for therapy and for understanding the pathophysiology of PD."[/I]

Things are going awry in our ability to synthesize amino acids but what is causing that?