Synucleinopathies
Recent clinical, regulatory, research and industry developments relating to this disease.
Synaptic vesicle-omics in mice captures signatures of aging and synucleinopathy.
Synaptic sabotage: How Tau and α-Synuclein undermine synaptic health.
Gut microbiota produces biofilm-associated amyloids with potential for neurodegeneration.
Ageing-Related Neurodegeneration and Cognitive Decline.
Overlaps and divergences between tauopathies and synucleinopathies: a duet of neurodegeneration.
Synaptic Involvement of the Human Amygdala in Parkinson's Disease.
What's happening now
An analyst briefing on current research, clinical, regulatory and industry activity surrounding this disease.
- 1 clinical trial expected to report results, the earliest in Q3 2028.
Clinical MilestonesViewHide
- 2026-07-07A Phase 2 Randomized, Placebo-Controlled Clinical Trial to Assess the Safety and Efficacy of Donanemab in Participants With Early Cognitive Decline, at Least One Core Clinical Feature of Dementia With Lewy Bodies, and Confirmation of Alpha-Synuclein and Amyloid Co-pathologyResults expected Q3 2028
- 2026-12-31Efficacy and Safety of Rasagiline in Prodromal Parkinson's DiseaseWithdrawn
- 2026-12-31ClinicalEfficacy and Safety of Rasagiline in Prodromal Parkinson's DiseaseWithdrawn
- 2026-07-07ClinicalA Phase 2 Randomized, Placebo-Controlled Clinical Trial to Assess the Safety and Efficacy of Donanemab in Participants With Early Cognitive Decline, at Least One Core Clinical Feature of Dementia With Lewy Bodies, and Confirmation of Alpha-Synuclein and Amyloid Co-pathologyResults expected Q3 2028
Clinical trials
The current development programme across all trial phases.
Research activity
Key research shaping understanding of this disease, combining the latest publications with the most influential evidence.
Major themes8
- Synucleinopathies6
- alpha-Synuclein3
- Parkinson Disease3
- Alzheimer Disease2
- Tauopathies2
- Aging1
- Amyloid1
- Biofilms1
Leading journals6
- Nature communications2
- Acta neuropathologica1
- Biomolecules1
- Cell death & disease1
- eLife1
- International journal of molecular sciences1
Leading researchers8
- Agúndez JAG1
- Ahmad S1
- Alafuzoff I1
- Alkorta-Aranburu G1
- Alonso-Navarro H1
- Alvarez-Erviti L1
- Antelmi E1
- Astillero-Lopez V1
Affiliations (unnormalised)6
- Brain and Mind Research Institute1
- California Institute of Technology1
- Center for Neurodegeneration and Experimental Therapeutics1
- Chalmers University of Technology1
- CHUAC-Complejo Hospitalario Universitario de A Coruña1
- Clínica Universitaria and Medical School1
Disease biology
Key proteins & gene products studied in this disease. Number shows shared papers.
Related conditions
Diseases frequently studied alongside this one. Number shows shared papers.
Disease profile
A grounded synthesis of the condition — overview, causes, mechanism, risk factors and current standard of care.
Synucleinopathies are a group of neurodegenerative disorders characterized by abnormal deposition of alpha-synuclein in dopaminergic neurons and glial cells in the brain. This protein aggregation produces Lewy bodies, Lewy neurites, melanin granules in the substantia nigra and locus coeruleus, and glial cytoplasmic inclusions. Prominent examples include Parkinson disease, Lewy body disease with dementia, and multiple system atrophy.
The grounding supports a genetic association with mutation in the SNCA gene on chromosome 4. It also indicates that abnormal alpha-synuclein is central to disease development, but does not support a single external cause for the group as a whole.
The core mechanism is abnormal alpha-synuclein accumulation in neurons and glia, with pathological aggregation into Lewy bodies, Lewy neurites, and glial cytoplasmic inclusions. Review abstracts further link abnormal alpha-synuclein to selective and progressive neuronal death through mitochondrial impairment, lysosomal dysfunction, altered calcium homeostasis, and early synaptic dysfunction. The literature also notes early inflammation and cross-seeding interactions with tau as part of overlapping neurodegenerative mechanisms.
Aging is a co-studied mechanism and is supported as a factor associated with synucleinopathies. The grounding also supports genetic susceptibility through SNCA mutation.
The supplied grounding does not describe treatment standards for synucleinopathies. It only indicates that the literature covers diagnosis and pathology, without supporting specific therapeutic modalities or drug classes.
AI-generated summary grounded in MeSH and 4 peer-reviewed sources. Informational only — not medical advice. Generated 2026-07-07.
Reference
Authoritative identity, definition & identifiers.
Neurodegenerative disorders involving deposition of abnormal ALPHA-SYNUCLEIN in dopaminergic neurons and glial cells in the brain. Pathological aggregations of alpha-synuclein proteins results in LEWY BODIES and Lewy neurites; melanin granules in the SUBSTANTIA NIGRA and LOCUS COERULEUS; and glial cytoplasmic inclusions. Synucleinopathies are associated with mutation in the ALPHA-SYNUCLEIN (SNCA) gene on chromosome 4. PARKINSON DISEASE; LEWY BODY DISEASE with dementia; and MULTIPLE SYSTEM ATROPHY are prominent examples of synucleinopathy.
- Disease identity & definition — NLM Medical Subject Headings (MeSH), public domain
- Clinical trials — ClinicalTrials.gov (U.S. National Library of Medicine)
- Research activity — Europe PMC (EMBL-EBI) + OpenAlex-derived paper links
- Related entities are derived from literature co-mention (studied together) — associative, not causal.