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PSP: being orphan for drugs, the tracer at least marks for discrimination

PSP is is a rare brain disorder of the atypical parkinsonism group, characterized by four-repeat tau aggregates in neurons (neurofibrillary tangles) and glia in specific basal ganglia and brainstem areas. A thorough literature review has led scientists to hypothesize that genetic and/or environmental factors contribute to its development. It is likely that inheritance of the H1/H1 tau genotype represents a predisposition to develop PSP requiring other environmental or genetic factors. Usual symptoms are loss of balance, blurred vision and uncontrolled eye movement, slurred speech, cognitive decline and mood changes. The disease worsens over time, and there is no cure. Often, PSP symptoms are similar to Parkinson’s disease and dementia, making it hard to diagnose. PSP can only be definitively diagnosed post-mortem by examining region-specific tau deposits in the brain. Future interventional trials targeting tau in PSP would strongly benefit from biomarkers to validate the specific presence of the tau deposits and to monitor treatment response during therapy.

A large body of neuroimaging research has been conducted over the past twenty years, proposing different structural MRI and molecular PET/SPECT biomarkers for PSP. These include measures of brainstem, cortical and striatal atrophy, diffusion weighted and diffusion tensor imaging abnormalities, [18F] fluoro-deoxyglucose PET hypometabolism, reductions in striatal dopamine imaging and, most recently, PET imaging with ligands that bind to tau. Researchers have discovered a novel radioligand that can effectively differentiate progressive supranuclear palsy (PSP) from similar brain disorders, allowing for earlier and more reliable diagnosis of the disease. Presented at the Society of Nuclear Medicine and Molecular Imaging’s 2019 Annual Meeting, these findings bring physicians a step closer to being able to definitively diagnose PSP with imaging rather than waiting for confirmation upon autopsy. Lead author is Matthias Brendel, MD, MHBA, at Ludwig-Maximilians-University of Munich, GermanyCurrently.

In the study, researchers utilized a novel second-generation radioligand, 18F-PI-2620, to evaluate patients with suspected tau pathology in clinically diagnosed PSP. Seventeen patients with probable or possible PSP underwent 18F-PI-2620 PET imaging at four different health care centers, along with 10 healthy control patients and 7 disease control patients who had multi-system atrophy, Parkinson’s disease or Alzheimer’s disease. Standardized uptake value (SUV) ratios of 18F-PI-2620 in predetermined brain areas were obtained and compared between the PSP, healthy control and disease control patients. In addition, disease severity, measured by the PSP rating scale, was correlated with PET findings. A significantly elevated mean 18F-PI-2620 SUV ratio was found in the globus pallidus and the substantia nigra areas of the brain in the PSP patients as compared to the healthy control group. In contrast, the disease control group showed similar or only slightly elevated SUV ratios when compared to the healthy control group.

Furthermore, results showed that even patients with low disease severity already had significantly elevated 18F-PI-2620 uptake in the globus pallidus when compared to the healthy control group. The team deems that giving drugs like riluzole failed to improve conditions like PSP, their radioligand may give them an hint on the development of a true pharmacological agent. Dr. Brendel commented his work: “My colleagues and I were able to detect an elevated signal in the majority of evaluated PSP patients and could clearly discriminate the PSP group from healthy controls and disease controls. Importantly, PSP patients at early disease stages also revealed an elevated PI-2620 signal, which points at the suitability of this ligand as an early PSP biomarker. Detection of tau in PSP patients by PI-2620 could play a role in future anti-tau trials for this disease, and molecular imaging could serve to select the right patients for targeted therapies”.

  • edited by Dr. Gianfrancesco Cormaci, PhD, specialist in Clinical Biochemistry.

Scientific references

Ali F, Josephs K. Expert Rev Neurother. 2018; 18(7):603.

Whitwell JL et al. Mov Disord. 2017 Jul; 32(7):955-971.

Rampello L et al. Neurobiol Dis. 2005 Nov; 20(2):179-86.

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Dott. Gianfrancesco Cormaci
Dott. Gianfrancesco Cormaci
Laurea in Medicina e Chirurgia nel 1998, specialista in Biochimica Clinica dal 2002, ha conseguito dottorato in Neurobiologia nel 2006. Ex-ricercatore, ha trascorso 5 anni negli USA alle dipendenze dell' NIH/NIDA e poi della Johns Hopkins University. Guardia medica presso la casa di Cura Sant'Agata a Catania. In libera professione, si occupa di Medicina Preventiva personalizzata e intolleranze alimentari. Detentore di un brevetto per la fabbricazione di sfarinati gluten-free a partire da regolare farina di grano. Responsabile della sezione R&D della CoFood s.r.l. per la ricerca e sviluppo di nuovi prodotti alimentari, inclusi quelli a fini medici speciali.

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