A reader just commented, “What other diseases can mimic PSP?” Below is a pretty exhaustive list of things that can cause vertical gaze palsy*, the most specific** diagnostic hallmark of PSP. Most of these disorders don’t mimic the whole classic PSP syndrome, but even PSP doesn’t do that in many cases. Keep in mind that most of these mimics have other features besides the gaze palsy that make them very unlikely to actually be confused with PSP in practice.
The disorders with specific treatment (though maybe not cures) have three asterisks ***.
*”Palsy” in general means weakness (not tremor, as popularly thought). In the setting of PSP, palsy refers to a limitation of the range of voluntary eye movements.
**The “specificity” of a diagnostic sign is technically the fraction of the people without the disease who don’t have the sign. In other words, specificity = [true negatives] divided by [true negatives + false positives].
DISORDERS WITH VERTICAL GAZE PALSY IN AT LEAST SOME CASES
This morning I received an email from a CurePSP support group leader in Texas forwarding a local newspaper clipping about a young girl in Taiwan with a genetic metabolic defect of the brain who had received a form of gene therapy. She asked if that approach could be of potential use against PSP.
Here’s my answer:
For decades, a routine neuroscience laboratory tool has been to inject the brain with a harmless virus, called a “vector,” carrying a gene to induce brain cells to manufacture that gene’s protein product. This has been useful in PSP research. Before long, the same idea could become a treatment for patients with neurodegenerative diseases. The main drawback is that it requires a neurosurgical procedure to inject the virus with the therapeutic gene into the specific spot(s) in the brain where it’s needed.
This approach has worked in early-phase trials in people with Parkinson’s disease, where cells that make dopamine are degenerating, and is continuing safety studies in PD. The gene in those trials encodes the enzyme AADC (aromatic amino acid decarboxylase), which controls dopamine’s rate of production. AADC mutations do not occur in PD, but the girl in Taiwan who received the gene therapy was suffering from an inherited deficiency of AADC, causing delayed neurological development.
This sort of gene therapy, but using MAPT, the gene for the tau protein, has been used in PSP research to produce a rat model for use in testing new treatments. The company sponsoring the AADC deficiency trial in Taiwan is developing an MAPT gene therapy for the rare form of frontotemporal dementia caused by mutations in MAPT, called FTDP-17. Unfortunately, PSP, unlike AADC deficiency or FTDP-17, is not caused by a single mutation in a known gene, so it would not be amenable to having that gene replaced by this sort of gene therapy. It’s true that PSP, like PD, includes a dopamine deficiency, but PSP would not respond to AADC gene therapy for the same reason it doesn’t respond to L-DOPA (which is converted by the body into dopamine): the brain cells on which dopamine acts degenerate in PSP.
The hopeful note, however, is that if a compound such as a growth factor protein or an anti-sense oligonucleotide (ASO) is found to help PSP, a gene for that compound could, in theory, be inserted into a viral vector and injected into the brain. That could provide a steady, lifetime supply of the compound.
Today is Martin Luther King Day, and here’s one of his best quotes, from 1968:
“We must accept finite disappointment, but never lose infinite hope.”
Fast-forward to the 1980s, early in my career as a neurologist mostly for patients with incurable movement disorders. I rapidly learned that besides objective diagnosis and treatment, my agenda at patient visits should include an old-fashioned pep talk along with an update on research. Now, I had grown up in a culture where such “touchy-feely,” subjective things were far subservient to scientific thinking, and my medical education was no different. So, once I was out in the real world of patient care, it was kind of a revelation to discover that a simple, subjective appeal to hope could sometimes alleviate more suffering than any medication, therapy or surgery I could prescribe.
Fast-forward again to 2004, at which point I had been CurePSP’s Clinical and Scientific Director for 14 years, and a new CEO named Richard Zyne arrived. He was an ordained minister who spent his career mostly with non-sectarian, non-profit organizations. As a clergyman, he well knew the value of hope in helping people deal with adversity, and he quickly made “Because Hope Matters” CurePSP’s tagline.
I’ll admit I was skeptical at first. I thought that providing hope was the doctor’s job at an individualized, “retail” level in the exam room and that CurePSP should support research, educate patients and clinicians, and help find ways to bring the best available care to all who need it. But working with CurePSP showed me the value of a national organization with multiple communication platforms in reassuring patients and families that scientific understanding of PSP is advancing, that similar diseases are slowly yielding to new treatment, that more researchers and journal articles are devoted to PSP than ever, and that a well-run non-profit organization is in their corner. In other words, I again discovered that hope matters, but now at a more “wholesale” level.
The idea for this blog post entered my mind from the proximity of MLK Day and my post from four days ago, where I reported the failure of one PSP drug candidate but offered hope for five others currently in clinical trials. In fact, regular readers of this blog know that I try to infuse hope into every post rather than merely reporting the news objectively. For the ability to understand the value in that, I thank my patients, Richard Zyne – and Dr. King.
I have some bad news. Another experimental drug has failed to slow the progression of PSP. The double-blind Phase 2 trial of RT-001 in 40 participants took place in Munich, Germany. The company, BioJiva, has given me permission to discuss this ahead of their press release.
RT-001 has a unique mechanism of action. It’s based on the ample evidence that a major part of the problem in PSP is an attack on brain cells’ membranes by “reactive oxygen species.” ROS, a product of dysfunction of the mitochondria, damage the fatty acids, a major component of cell membranes. The drug is one of those fatty acids, linoleic acid, but with a twist. Two of the hydrogen atoms in the molecule are replaced by deuterium, which is hydrogen with an extra neutron in its nucleus. (Water made with deuterium instead of hydrogen is called “heavy water.”) The drug is incorporated into the membranes as if it were ordinary linoleic acid, but the two deuteriums protect it against attack by the ROS.
Sound crazy, you say? Naïve, maybe? Well, it may actually work in another disease with too much ROS activity, amyotrophic lateral sclerosis! BioJiva announced last year that an early-phase trial in ALS gave favorable, albeit undramatic results, with a 23% slower rate of decline relative to the placebo group. So, the company will continue to pursue work with RT-001 in ALS, but not in PSP.
But take heart, PSP community. There are still five PSP neuroprotection trials in progress using fasudil, TPN-101, NIO-752, sodium selenate, and AZP2006. Then, of course, there are multiple trials of “symptomatic” treatment. See my recent post for details.
Which of those five PSP neuroprotection candidates is most likely to work? I wish I (or anyone) knew enough about the molecular and cellular abnormalities underlying PSP to answer that question.
Disclaimer: I don’t own any stock in BioJiva or have any other financial relationship with them. Their Chief Medical Officer gave a presentation on the then-ongoing trial at CurePSP’s “Neuro2022” symposium in New York in October, where I was one of the organizers and moderators.
Two full weeks since my last post – holiday activities, don’t you know, starting on December 21 with a solstice party at the home of an eccentric friend. I see that my blog viewership has declined precipitously in the past week, so I’m happy that you all have better things to do at holiday time than to read about PSP. Don’t we all wish that the disease itself would take a few days off, too?
My re-emergent thought is about the famous “hummingbird sign.” On an MRI scan in the sagittal plane – that’s as if you sliced someone down the middle and looked at the cut surface – the brainstem sort of looks like a side view of a hummingbird.
In the MRIs above, the nose is on the left. In the lower images, the arrows stop just short of the indicated structures so as not to obscure them. Note the progressively thinner, sleeker midbrain (the hummingbird’s head and beak) with retention of the plump pons (the belly, which is plumper than than that of a real hummingbird).
Now here’s the issue. The appearance of the hummingbird sign isn’t as closely related to PSP as has been implied by many. There are just too many false positives and false negatives.
The false positives mostly occur in people with normal-pressure hydrocephalus, a condition where the fluid-filled spaces in the brain (the “ventricles”) enlarge because of an obstruction in the re-absorption of the fluid into the bloodstream. This stretches the fibers adjacent to the ventricles, impairing control of gait, cognition and the bladder. It also presses down on the midbrain, producing the hummingbird sign. Then there are those individuals with corticobasal degeneration where the features resemble PSP (“CBS-PSP”). They can also have a hummingbird sign.
The false negatives occur in the first couple of years after the initial symptoms. They also occur if the MRI is mis-aligned on the brain or the head is a little rotated, producing an allegedly midline cut that’s actually a couple of millimeters to one side. That means that the thinnest part of the midbrain, which is in the midline, isn’t shown in the image.
You should also know that the hummingbird sign isn’t just about a thin midbrain. A normal pons is also part of the sign. That’s because in multiple system atrophy and a few rarer disorders, both the midbrain and pons become thinner. But in PSP, it’s mostly the midbrain that does so.
I think that in the next year or two, a test of the tau protein in spinal fluid, blood or a tiny punch biopsy of skin will provide a much more accurate diagnosis of PSP than the hummingbird sign. Soon thereafter we will probably have a PET technique that does the same. Then, clinical treatment trials can be accomplished faster because they won’t have to compensate for the statistical noise produced by participants with a false positive diagnosis. In fact, all sorts of research on PSP will become much more powerful if people without PSP can be excluded.
I know that some of my posts are too technical for some of my readers, so I’ll make amends right now. An important paper just appeared in the journal Neurology and Therapy called “The Lived Experiences of People with Progressive Supranuclear Palsy and Their Caregivers.”
The nine authors were led by Dr. Gesine Respondek, a well-published PSP expert formerly at Hannover Medical School in Germany and now at Roche Pharmaceuticals. The others are a diverse group from five different European medical institutions, two patient advocacy organizations and the study’s sponsor, the Belgian drug company UCB Biopharma. They performed one-hour interviews of 21 patient/caregiver pairs, 7 patient organization representatives, 21 nurses and 42 neurologists in France, Germany, Italy, Japan, Spain, the UK and the US. The patients and caregivers also completed smartphone-based, 7-day diaries with photos and formal daily questionnaires. The analysis used a qualitative approach rather than attempting to fit the subjective information into a standard statistical model used in most medical research.
The study identified barriers to optimal care, the emotional responses to being a patient or a caregiver, and major “pain points.” The areas identified as important were:
delays in seeking medical advice for the initial symptoms because of apathy or misattribution of the symptoms by the patient or family
lack of awareness of PSP by non-neurologists
delays in even the neurologist suspecting PSP because of delayed appearance of downgaze difficulty or other hallmarks
a feeling of being overwhelmed by the diagnosis and its implications
delays in being referred by the general neurologist to a movement disorders specialist
diagnostic uncertainty even by the movement disorders specialist because of the overlaps between PSP and other candidate diagnoses
absence of objective diagnostic tests
a lack of empathy by the neurologist
frustration in having to settle for symptomatic treatment rather than disease-modifying treatment
the problem of being “no longer you”
the loss of independence in daily activities
lack of consistency in the rating and monitoring of symptoms
lack of guidelines and quality care standards for PSP management
stresses in confronting the end of life
caregivers feeling frustrated, sad, lonely, guilty and unsupported
The most important stresses among these related to the delays in receiving a correct diagnosis. The countries differed in some areas with Japan offering the best support, information and home care.
The authors concluded with these recommendations:
More countries should create patient organizations dedicated to PSP.
Time allotted for consultations should be longer to allow the clinician to better educate the patient/caregiver. If this is not possible, then providing formal follow-up time by phone or video would be a good substitute.
To assist in the above, one of the shorter versions of the PSP Rating Scale should be widely adopted by neurologists in order to provide patients with an quantitative measure of their status within the time allotted at the visit.
At-home follow-up by a nurse specialized in parkinsonism, when financially feasible, would help.
Closer collaboration between patient organizations and clinicians should be facilitated.
More information should be available on “financial support, life expectancy, nutrition and tube feeding, and preparation for end-of-life.”
There should be better access to support for patient and caregiver in the form of adult day programs, support groups, respite care, home health care, social work, caregiver training and psychological support.
Tele-health forms of occupational therapy should be available.
Clinicians should be honest and open with the patient and caregiver about the unpleasant truths and the uncertainties.
The needs of the caregiver should be as important as those of the patients to clinicians, support organizations, insurors and policymakers.
As my own editorial response, I’ll say that:
Many of these recommendations are for services already available in the US via CurePSP and in the UK via the PSP Association. But funding limitations at these charities limit their reach.
CurePSP and the PSPA already offer many forms of layperson and professional education where funding is not an issue. They just have to get it to the right people.
Creating new or more educational materials for clinicians who can read English is not a priority. We just need to grab their attention and convince them to devote some time and energy from their busy schedules to learning the material. Providing the materials in other languages would also help.
CurePSP’s Centers of Care network, which is only just getting started in earnest, is attempting to address many of the deficiencies on the part of professional education and access to care. The best example is its “Best Practices” paper advising on treatment options and published last year.
I hope that there can be a radical change in how most physicians and insurers see PSP. The current, “Oh, PSP is just a disease that old people get, and you’ve got to go sometime, and there’s nothing to be done.” has to change to, “PSP is a disease that reduces the quality and quantity of one’s retirement years and its sufferers and their families can benefit in many ways — both psychological and physical — from better access to care, faster diagnosis, and delivery of well-informed and empathetic symptomatic management.”
Maybe nothing is more boring to patients and their families than squabbles among doctors about how to classify diseases. But here goes.
You may have read that PSP is one of the “frontotemporal dementias.” The FTDs are an umbrella category of diseases with deficits involving degeneration of the frontal and temporal lobes. The results are trouble planning, forming new ideas, multi-tasking, obeying rules and adapting to circumstances. Some types of FTD also (or mostly) have problems with speech and language. Yes, PSP includes some of those things to some degree, but unfortunately, that’s only one of many parts of PSP.
The protein aggregating in the brain cells in the various FTDs can be tau, as in PSP, but only in a minority. Even in those few with tau, the distribution of the aggregates is different from that of PSP. The majority of FTDs don’t even have tau – instead, they have the proteins TDP-43, FUS or ubiquitin. So, it has always irked me to hear PSP classified as an FTD.
This replaces a set of criteria from 1996, antedating modern methods of tissue staining (necessary for viewing through the microscope) certain observations about the pathology of PSP. Now, here’s the critical part: the new criteria don’t require, or even accept, abnormalities in the temporal lobes in support of the diagnosis of PSP.
The new criteria, called the “Rainwater Charitable Foundation Criteria” for the philanthropy funding the project, are very simple. They require both of these:
Neurofibrillary tangles or pre-tangles, at least mild in frequency, in two or more of the following regions: globus pallidus, subthalamic nucleus and substantia nigra
Tufted astrocytes, at least mild in frequency, in either peri-Rolandic cortices or putamen
Neurofibrillary tangles: mature aggregates of tau protein
Pretangles: aggregates of tau protein that aren’t (yet) sufficiently well-formed to be called tangles
Globus pallidus: part of the basal ganglia, an important area for control of movement
Subthalamic nucleus: another movement-control area, a cluster of brain cells so-called because it’s just under the thalamus
Substantia nigra: yet another movement-control area, the one where dopamine is made; It’s also a critical one for Parkinson’s.
Tufted: containing a type of tau aggregate with a sort of fluffy appearance
Astrocytes: the main type of glia, which are non-electrical brain cells
Peri-Rolandic cortices: the folds of the cerebrum running down each side of the brain in front of and behind a long in-folding called the Rolandic fissure. The pre-Rolandic cortex is part of the frontal lobe and serves motor control. The post-Rolandic cortex is part of the parietal lobe and serves the sense of touch.
Putamen: another movement control area of the basal ganglia
The fact that involvement of the temporal lobe is so mild and inconsistent in PSP as not to merit a place in the new diagnostic criteria should finally put an end to the notion that PSP should be classified as one of the fronto-temporal dementias.
I was gratified to discover recently that the Memory and Ageing Center at UCSF, possibly the leading such institution in the world, now specifically states on its website’s home page that PSP, while sharing some symptoms with the FTDs, is not one of them.
So, why does this matter? Because PSP is sufficiently different from the FTDs that it deserves to be researched and treated on its own. Its sufferers and their families need a type of support not generally relevant to the FTDs. Similarly, those serving the urgent and important needs of the FTD community should not be distracted by efforts aimed at PSP.
A bombshell hit the news yesterday (11/20/22) about a breakthrough treatment for Alzheimer’s disease. But the drug company announced the same news two months ago in the form of a press release. Today’s story was merely about a formal presentation of the results at an Alzheimer’s conference that added some important safety data. Here’s my blog post from September.
The drug is called lecanemab, and as its last three letters indicate, it’s a monoclonal antibody – in this case directed against the beta-amyloid protein. That’s present in an abnormal, aggregated form in brain cells in Alzheimer’s but not in PSP. In the trial, the antibody solution was infused intravenously every two weeks for 18 months and compared with a group of participants receiving placebo infusions. The news was that lecanemab slowed the rate of worsening of Alzheimer’s by 27%. This is great news from the PSP standpoint because it’s the first time that a monoclonal antibody was shown to slow progression of any neurodegenerative condition, even if it’s a different one. We call that a “proof of principle.”
Today’s new information on the drug’s safety was most notable for a potentially serious issue called hemorrhagic encephalitis. That’s where areas of the brain tissue undergo swelling and/or bleeding. That combination is evidence of inflammation, the equivalent of a very sore arm after a Covid shot. Among the 898 participants with AD who received active lecanemab over the 18 months of the trial, 13% had swelling, but for the 897 receiving placebo, the figure was 2% – a major difference. For bleeding, the proportions were 17% for lecanemab and 9% for placebo – a minor difference. Fortunately, none of those participants suffered important or permanent symptoms from the swelling or bleeding, which in most cases would not even have been suspected without the trial’s routine brain MRIs, and in all cases resolved in a few weeks. However, one wonders how serious the problem could hypothetically be in a tiny percentage of people — too small a fraction to be detected in the 897 on lecanemab in this study.
The group on active lecanemab was a bit more likely than the placebo group to report a variety of serious side effects unrelated to brain swelling or bleeding: 14% vs 11%; and the lecanemab patients were more likely to drop out of the study because of other, assorted side effects: 7% vs 3%.
Now the FDA and Medicare/Medicaid have to decide if they’ll approve this treatment or if the cost (whatever that might turn out to be) and side effects outweigh the benefit. Or, they may require another large trial first.
So, the takeaway for those with PSP is that it’s possible to modestly slow the rate progression of a neurodegenerative disease with a monoclonal antibody treatment with probably only mild risk. The numbers about the hemorrhagic encephalitis are not to be ignored. But I think that if a hypothetical treatment for PSP gave similar risk and benefit, and the out-of-pocket cost is affordable, I think the majority of people with PSP would ask where to sign up.
If PSP is an orphan disease, corticobasal degeneration (CBD) can’t even get into the orphanage. Like PSP, it’s a “pure 4R tauopathy”; it can resemble PSP in many cases; it leads to disability and death after a similar span of time; and it’s no more treatable. But its prevalence is about 10-20% that of PSP and it’s very difficult to diagnose in a living person. People fulfilling the accepted, published diagnostic criteria for the most common type of PSP (PSP-Richardson syndrome) actually have that disease at autopsy in over 90% of cases, but for CBD, the figure is less than 50%. That makes it hard to recruit a group of subjects for a drug trial — or any research — without other diseases influencing the result. That has put quite a damper on CBD research.
To add injury to injury, googling “CBD” reveals a lot more about cannabidiol than about corticobasal degeneration.
So, an objective diagnostic test for CBD would be great. Now, researchers mostly at Washington University in St. Louis (WUStL) and University of California, San Francisco (UCSF) have shown that two tiny fragments of the tau protein are less abundant in the spinal fluid of people CBD than in healthy people or those with PSP or three other rare tau disorders called argyrophilic grain disease, Pick’s disease and frontotemporal lobar degeneration associated with aggregation of TDP-43. They found no difference between CBD and Alzheimer’s disease or frontotemporal lobar degeneration with mutations in the tau (MAPT) gene, but in practice, those two disorders can be readily distinguished from CBD by other means.
The paper appears in the prestigious journal Nature Medicine and it’s open access, so I can provide you this file to download. The first author is Kanta Horie, PhD and the senior authors are Chihiro Sato, PhD and Randall Bateman, PhD, all of WUStL.
Panel “a” shows the tau protein. The four microtubule-binding domains are R1 to R4. The one whose inclusion or exclusion makes the difference between the 4R and 3R tauopathies is R2, which is encoded by the gene’s exon 10. The amino acids are numbered starting at the N terminus on the left. Two short stretches of amino acids, numbers 275 to 280 and 282 to 290, were the object of this paper’s analysis. N1 and N2 are two other sections, encoded by exons 2 and 3, respectively, that can be included or excluded in the finished tau protein.
Panel “b” shows the analysis of the 275-280 fragment of tau in the spinal fluid (CSF). The vertical axis is the ratio of the concentration of the 275-280 fragment divided by the concentration of total tau. The horizontal axis lists the tauopathies analyzed in this project. Each circle is one patient. The “box-and-whisker” plot shows, from top to bottom, the maximum value, the 75th percentile, the median, the 25th percentile, and the minimum value. The asterisks indicate the statistical significance of the comparison between the two groups at the ends of each horizontal line segment. One asterisk is a weak difference and four is the strongest. Pairs of groups without a horizontal line connecting them did not differ (i.e. the p value was greater than 0.05, meaning that any difference between them could have occurred by chance with a likelihood of more than 1 in 20).
Panel “c” shows the same thing, but for the 282-290 fragment of tau. The results are essentially the same as for the 275-280 fragment.
The odd thing is that the same analysis using autopsy brain tissue rather than spinal fluid gave a very different result: The values (i.e., the ratio of the fragment to total tau) was actually higher for CBD than for the other groups. The authors present various theories to explain this, but in any case, it does not detract from the diagnostic value of the spinal fluid results. Take a look and the brain tissue results:
So, what does this mean for people diagnosed with CBD, present and future? It means that if someone like a drug company has an experimental treatment that might help CBD, they could recruit a group of patients with a high level of confidence that they have excluded other diseases that could confound their results. That level of confidence is expressed as the “area under the receiver operating curve” or AUC. A previous post on this blog explains that statistic, which varies from 0.5 for a diagnostic test no better than a throw of the dice to 1.0 for a test that’s perfectly accurate every time. The AUC for this test to distinguish CBD from those other disorders (other than AD and FTLD-MAPT) is 0.800 to 0.889. That’s close to the figure for PSP using the neurological history and exam.
If this diagnostic test is confirmed (a big “if”) and enters use by researchers and drug companies, and if a drug company sees a route to profitability in so rare a disease, the only problem is finding enough patients with CBD for a trial. If CBD is 20% as common as PSP, and the new test for CBD is just as good as the present clinical diagnosis of PSP, then it will require five times the number of participating clinical test sites to fill a trial. But with international collaboration, it’s do-able.
Now, let’s hope that this test is adopted and that CBD is adopted.
The work was performed using rhesus monkeys, also called “macaques,” which have been productively and frequently used in research for over a century. The researchers injected abnormal tau protein from patients with PSP into the midbrain of two macaques. As controls, they injected normal tau from the brains of two people whose autopsies showed no neurological disease into the midbrain of two other macaques. The result was that starting six months later, the first group started to show abnormal control of walking and loss of performance on a cognitive task requiring opening a box containing a treat.
The deficits progressed, and after another 12 months, the animals were euthanized. Brain tissue of the two recipients of the abnormal tau showed the same sort of tau aggregation seen in human PSP. Also, crucially, the tau abnormality had spread to several areas known to be connected to the original injection. Those areas — the putamen, caudate, globus pallidus and thalamus — are among the main sites of involvement in human PSP. They must have received the abnormality from the injection site through axons and across synapses, not by mere proximity. The two control macaques had neither symptoms nor brain abnormalities at autopsy.
Similar experiments have been done with mice over the past decade with similar results, but:
The mice did not display the full range of PSP-related brain changes that occurred in the monkeys.
The mouse brain’s simpler circuitry and much smaller size do not closely mimic the “environment” in which the abnormal tau spreads in human PSP.
The types of normal tau in the brain, a mix of 3R and 4R, is like that of humans, while normal mice produce only the 3R type. (“R” is a stretch of amino acids in the tau protein that allows it to attach to the brain cells’ microtubules. The number is how many such stretches exist in the tau molecule.) This suggests that macaques and humans share a similar genetic control of tau production.
The complexity of monkeys’ normal movements and cognitive processes more closely resemble those of humans, allowing more valid extension of the experimental observations to humans and their diseases. This complexity also allows a finer-grained evaluation of the effects of the experimental intervention.
The authors point out that while only four macaques were necessary to demonstrate this result, larger numbers would be needed to confirm the findings and to turn this model into a practical research tool. Once that happens, many research labs the world over could use this technique in studying PSP and testing drugs designed to slow, stop or reverse its progression.
Now here’s the issue at hand: The last line of the paper is:
“ . . . our results support the use of PSP-tau inoculated macaques as relevant animal models to accelerate drug development targeting this rare and fatal neurodegenerative disease.”
At one level, they are probably right: using macaques in research would bring a cure for PSP faster than using mice. But some people oppose the use of animals of this level of intelligence in scientific research, no matter the benefit to humans. I’m interested in your opinion: should macaques be used in PSP research?
No, I don’t know how many macaques might ultimately be needed. Nor do I know how much sooner a cure would be found compared to the present practice of using only rodents. So, try to provide an opinion that transcends those important specifications.
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