A couple of weeks ago I posted my curated list of the top 10 PSP-related research developments of 2025. They appeared in two installments on 12/31/25 (#1-5)
and 1/1/26 (#6-10).
Clearly inspired by my effort, the publication “Parkinson’s News Today” (PNT) has done the same for Parkinson’s disease. Their article is very well supplemented with links to both basic explanations and to the PNT articles themselves. Those PNT items link, in turn, to original journal articles and to press releases from drug companies or research institutions.
PNT is owned by a for-profit medical communications company and its on-line publication is monetized by advertising, mostly from drug companies. So be aware that their choice of what’s important may be biased in favor of drug companies’ products and scientific narratives. No such concrete instances have hit me over the head, but the potential for a conflict of interest is there.
Armed with that caveat emptor, you can learn a lot from this list, which is numbered from least to most important. Here are my annotations for each item, pointing out the relevance, or lack thereof, for PSP:
#10: Virus long thought harmless may trigger Parkinson’s
The brain tissue in PSP looks very similar to that of “post-encephalitic Parkinsonism” (PEP), which was quite common from the 1920s to 1950s. Both feature tau-based neurofibrillary tangles and attack the basal ganglia, but PEP is static over decades. It appears to be a immunologically-based , residual effect of a brain infection called “von Economo’s encephalitis” or “encephalitis lethargica.” The virus itself has never been isolated or identified. The disease overlapped, but is different from, the great flu pandemic following World War I. Otherwise, despite ample search, there’s little to no evidence that any virus can cause PSP.
#9: Scientists develop weekly injectable implant for Parkinson’s treatment
The implant (actually a viscous, intra-muscular, self-injected liquid) provides levodopa/carbidopa (LD/CD) for a week. Unfortunately, most people with PSP respond little or not at all to levodopa/carbidopa. However, in those with the PSP-Parkinsonism subtype and few with other subtypes, there can be a useful response for a few months of daily dosing. While those with PSP who do respond don’t need a long-acting form, avoiding having to take pills could be a major advantage for those with swallowing difficulty.
#8: DBS plus exercising may rewire Parkinson’s brain
The brain, even in older persons, can route its circuits around areas of damage, especially if those circuits are used often. That’s called “exercise” or “physical/occupational therapy” or just “practice,” (note my sarcasm) and it does work. This is true in PSP as well as in PD. But deep brain stimulation (DBS), at least the kind used in PD, does not work in PSP. That’s because the brain areas that are overactive in PD simmer down in response to DBS. But in PSP, those areas are part of the degenerative process itself, and are underactive. But to repeat: Informal physical activity and formal physical/occupational therapy do work in PSP. They should be an important part of the daily routine, assuming that one’s physician decides that any balance problems, osteoporosis, or cardio-pulmonary disorders are not contraindications.
#7: FDA approves bilateral Exablate Neuro treatment for Parkinson’s
Exablate is the brand name for a device that focuses destructive ultrasound beams on those over-active brain areas of PD. (It usually appears in the literature as “focused ultrasound” or FUS.) So, the idea is same as DBS, but FUS produces a permanent lesion that can’t be adjusted by the doctor based on the patient’s response. But its advantage of FUS over DBS is no hardware in the head, wires under the skin, pacemaker device in the chest, periodic battery changes, or explanations at metal detectors. Unfortunately, the FUS lesion locations used in PD would not work in PSP, but novel lesion locations could, in principle, be discovered for PSP for problems like balance, speech or cognition.
#6: Dosing starts in trial of anti-inflammatory therapy for Parkinson’s
PNT’s news item reporting the start of this single-center, Phase I trial appeared in March, as their blurb states, but I’ve got an update for you. The drug’s safety and tolerability were satisfactory but trial, with only 30 patient and one month’s observation, was not powered to demonstrate efficacy. The sponsor company, Ventus Therapeutics, has now started a Phase II trial for PD at 23 US sites. The drug, called VENT-02, targets NLRP3, a receptor protein activated by stress signals in the microglia, the brain’s equivalent of white blood cells. That could be relevant to PSP, where microglia help spread the abnormal tau protein through the brain and otherwise mediate the brain inflammation of PSP.
I’ll cover items #5 through #1 tomorrow or whenever my week’s chores permit.
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