Aren't the dementia symptoms greatly magnified by the lack of mobility in the first place?

If we could get this kind of treatment early it might alleviate the need for dementia treatment.

I would say, maybe the other way around - gait is very much a cognitive task (think of all the compute power w/ reinforcement learning to get a robot to stand up or balance a stick). but it is probably a self-reinforcing cycle.

That being said, from DBS clinical series - we know the technology helps w/ limb rigidity, bradykinesia and tremor. It helps initially with gait but sometimes the gait declines despite DBS and meds, say, roughly a decade after implant (even as the upper limb symptoms stay well treated).

My father had Parkinson's and in my experience the lack of agency he had when trying to do daily tasks even other than walking was a real mind-killer. He was dependent on my mom (and later caretakers and skilled nursing facility) to do anything like feeding, toileting etc. Obviously when he was later bedridden mostly due to the inability to move, it probably drove him even more crazy.

He decided early on to never get this treatment and I feel sad to this day that he couldn't have lived a happier last few years.

My father was disqualified from getting DBS due to concerns around amplifying his dementia. Had I known then what I know now, I would have gladly signed a waiver, because DP has completely destroyed his body and mind.

Disagreed, exercise of all kind is known to help with neuroplasticity, complex movements such as dancing and compound lifts even more so. I can easily see how being unable to do any of those things could at least contribute to mental decline.

As I understand the medical science, it all comes down to stimulating the brain and there is no harder stimulation than physical feedback. Lack of mobility means lack of the biggest source of brain stimulation, which leads to accelerated degeneration.

I think we're talking about 2 different things.

movement/neuroplasticity/physical stimulation absolutely helps - hence PT, exercise classes, etc have being an important part of treatment

My point is, though - the onset of decline in gait ability typical of Parkinson's patients, is a sign of a decline of cognitive ability because the ability to perform gait and all the inherent brain commands associated with gait, is very much a cognitive function as much as it is motor.

One can argue that good DBS therapy by helping keep patients active and engaged does, at least indirectly, help cognition in that sense. BUT - it is consider not to directly treat Parkinson's dementia if a patient is unfortunate enough to come down with that aspect of disease. i.e. it's not like we can switch the device on or fiddle around w/ the programming and the patient's cognition directly improves from the brain stimulation itself.

If the result actually holds up in clinical trials though this is still huge! Parkinson’s is absolutely debilitating and more common than ALS.

Results of their clinical trial look positive.

https://pubmed.ncbi.nlm.nih.gov/39289373/

Keep in mind that paper cited isn't really the clinical trial that shows improvements in symptoms. It just shows their device works and can record LFP properly....

The actual clinical results so far shows that the gizmo with recording is not necessarily worse than DBS devices that don't have recording ability. I don't know if they published those results in a paper yet, but it was shown in poster form at MDS congress in Philly.

Any idea what a clinical trial to approval roadmap might look like? Vested interest.

not sure - but it will likely be quicker because the software is sort of already built into current generation Medtronic devices. They are not trying to approve a whole new device, probably just the software that switches the device on/off.

That being said, there are also reasons at the moment (better imaging support/stimulation programming abilities) to sometimes choose a competitor device over Medtronic (namely Boston Scientific)

Better DSP/ML techniques might make this more effective, but uh...the Parkinson's research community has never been known to be great at math...just saying

DBS devices have been in the market for years already and helping patients. This is just an incremental improvement.

How does it work that it helps the motor symptoms?

And while it’s something if it doesn’t help with dementia it seems like it’s not addressing whatever is the root cause of dopamine deficiency

our understanding Parkinson's is that it can be described as a control system issue. The part of the brain affected (at least initially) by the disease is part of a network (the basal ganglia/cerebellar network) that evaluates environmental inputs and generates the output necessary for fine/precise motor control, amongst other things. So a Parkinson's patient cannot plan their movements as well and the main symptoms are slowness of movement, abnormal limb tone; yes tremor as well but the 1st 2 are what cause the most issues for most people (keep in mind, not everyone follows the textbook so there are subtypes that have more cognitive issues, i.e. hallucinations, executive dysfunction etc)

The stimulators seem to affect the signaling in that circuit (they are targeted by the implanting neurosurgeon to specific nodes in that circuit as best as targeting surgical technology allows) that seem to restore the ability to move well. Exactly why, no one knows. It's just a dumb signal at around 1-4 milliamps at 130-180 hz at those specific spots but presumptively it corrects some aberrant behavior in the whole network. It was observed in the '00s that recordings taken during or right after surgery often showed a strong peak at ~13-35 hz (give or take, but roughtly around 20 hz) during the disease state, and that's what Medtronic has been trying to target w/ these devices.

Of note - there actually isn't a system-wide dopamine "deficiency" - dopamine in general is fine for most of the body, it's just that the particular part of the brain that is affected happens to use dopamine as its signaling neurotransmitter so it's deficient in just that connection within the network.

Dementia is theorized to happen when the abnormal brain process spreads to other parts of the brain other than the substantia nigra (see the Braak hypothesis)