Here's the spin I'd put on it from the PD point of view.

Crucial to the pathogenesis of PD is the death of dopaminergic neurons, most importantly in the substantia nigra, but also in the rest of the brain and in the enteric nervous system. Even in one person there is no single cause: genetics, environment and diet all play a part. The effects of ageing are essential. Even added together all these processes would be insufficient to cause PD, except, perhaps, in extreme old age. To get the disease there needs to be a positive feedback mechanism. (Note "positive" here does not mean a good outcome but, rather, that the disease feeds on itself.) In PD this is performed by the misfolding of alpha-synuclein. Thus, rather than think of the cause or even the causes of PD, it is better to think of the disease as a process.

The import of the AD results is that a multi-pronged attack on all points in the process can slow the progression of the disease, even in those people who have symptoms bad enough to be diagnosed, to an extent where the brain's plasticity is sufficient for symptoms to be reversed.

If this hypothesis applies to PD, we need to identify, perhaps, 20 small wins. Things like exercise. The problem is that the clinical trial process is neither responsive nor sensitive enough to do this in a short period of time.

If we, PwP, are to get this soon, we need to work together now.

John