This review is from Melbourne and Prof. Finkelstein is one of the authors as he has been in a couple of ATH434 papers. In my opinion, there is not much from the point of ATH434 but it is good and positive that we get some MSA reports from scientists close to ATH. Most likely ATH is doing a lot of research as they tell in the annual report, but they are not publishing any. The latest paper about ATH434 is already 1 year old and even that was considered to be made by outsiders in spite of Finkelstein being one of the authors (ATH434 Rescues Pre-motor Hyposmia in a Mouse Model of Parkinsonism). Evidently, he is also in the PD primate study ATH got 1 million soon 3 years ago. Finkelstein has had an interest in GI symptoms in PD and in PD he published in 2021 an animal study: ATH434 Reverses Colorectal Dysfunction in the A53T Mouse Model of Parkinson's Disease. So I would expect that there will be later a study, perhaps related to the phase 2 studies, on how the ATH434 works in these severe gastric symptoms of MSA.

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Title & authors Abstract Conflict of interest statement Publication types LinkOut - more resources

Review

Neurobiol Dis

. 2023 Sep 13;106296.

doi: 10.1016/j.nbd.2023.106296. Online ahead of print.

Understanding the potential causes of gastrointestinal dysfunctions in multiple system atrophy

Colin F Craig ¹, David I Finkelstein ², Rachel M McQuade ³, Shanti Diwakarla ⁴

Affiliations expand

• PMID: 37714308

DOI: 10.1016/j.nbd.2023.106296Free article

Abstract

Multiple system atrophy (MSA) is a rare, progressive neurodegenerative disorder characterised by autonomic, pyramidal, parkinsonian and/or cerebellar dysfunction. Autonomic symptoms of MSA include deficits associated with the gastrointestinal (GI) system, such as difficulty swallowing, abdominal pain and bloating, nausea, delayed gastric emptying, and constipation. To date, studies assessing GI dysfunctions in MSA have primarily focused on alterations of the gut microbiome, however growing evidence indicates other structural components of the GI tract, such as the enteric nervous system, the intestinal barrier, GI hormones, and the GI-driven immune response may contribute to MSA-related GI symptoms. Here, we provide an in-depth exploration of the physiological, structural, and immunological changes theorised to underpin GI dysfunction in MSA patients and highlight areas for future research in order to identify more suitable pharmaceutical treatments for GI symptoms in patients with MSA.

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