SNCA — Alpha-Synuclein

SNCA — Alpha-Synuclein

Pathway Diagram

```mermaid
flowchart TD
SNCA["SNCA<br/>Gene"]
ALPHA_SYN["Alpha-Synuclein<br/>Protein"]
AGGREGATES["Alpha-Synuclein<br/>Aggregates"]
LEWY_BODIES["Lewy Bodies<br/>Formation"]

PLK2["PLK2<br/>Kinase"]
REP1["REP1<br/>Regulatory Gene"]
ASO["Antisense<br/>Oligonucleotides"]

PD["Parkinson's<br/>Disease"]
ALZHEIMER["Alzheimer's<br/>Disease"]
ALS["Amyotrophic<br/>Lateral Sclerosis"]
DEMENTIA["Dementia"]

NEURODEGENERATION["Neurodegeneration"]
INFLAMMATION["Neuroinflammation"]
DOPAMINE_LOSS["Dopaminergic<br/>Neuron Loss"]
MOTOR_SYMPTOMS["Motor<br/>Dysfunction"]

SNCA -->|"encodes"| ALPHA_SYN
ALPHA_SYN -->|"aggregates"| AGGREGATES
AGGREGATES -->|"forms"| LEWY_BODIES

PLK2 -->|"regulates"| SNCA
REP1 -->|"regulates"| SNCA
ASO -->|"inhibits"| SNCA

SNCA -->|"causes"| PD
SNCA -->|"associated_with"| ALZHEIMER
SNCA -->|"associated_with"| ALS
SNCA -->|"interacts_with"| DEMENTIA

LEWY_BODIES -->|"promotes"| NEURODEGENERATION
NEURODEGENERATION -->|"leads_to"| DOPAMINE_LOSS
DOPAMINE_LOSS -->|"causes"| MOTOR_SYMPTOMS

AGGREGATES -->|"triggers"| INFLAMMATION
INFLAMMATION -->|"exacerbates"| NEURODEGENERATION

style SNCA fill:#006494
style ASO fill:#1b5e20
style PLK2 fill:#4a1a6b
style REP1 fill:#4a1a6b
style PD fill:#ef5350
style ALZHEIMER fill:#ef5350
style ALS fill:#ef5350
style NEURODEGENERATION fill:#ef5350
style INFLAMMATION fill:#ef5350
style MOTOR_SYM

SNCA — Alpha-Synuclein

Pathway Diagram

<table class="infobox infobox-gene">
<tr>
<th class="infobox-header" colspan="2">SNCA — Alpha-Synuclein</th>
</tr>
<tr>
<td class="label">Symbol</td>
<td><strong>SNCA</strong></td>
</tr>
<tr>
<td class="label">Full Name</td>
<td>Alpha-Synuclein</td>
</tr>
<tr>
<td class="label">Chromosome</td>
<td>4q22.1</td>
</tr>
<tr>
<td class="label">NCBI Gene</td>
<td><a href="https://www.ncbi.nlm.nih.gov/gene/6622" target="_blank">6622</a></td>
</tr>
<tr>
<td class="label">Ensembl</td>
<td><a href="https://ensembl.org/Homo_sapiens/Gene/Summary?g=ENSG00000145335" target="_blank">ENSG00000145335</a></td>
</tr>
<tr>
<td class="label">OMIM</td>
<td><a href="https://omim.org/entry/163890" target="_blank">163890</a></td>
</tr>
<tr>
<td class="label">UniProt</td>
<td><a href="https://www.uniprot.org/uniprot/P37840" target="_blank">P37840</a></td>
</tr>
<tr>
<td class="label">Diseases</td>
<td>[Parkinson's Disease](/diseases/parkinsons-disease), [Dementia with Lewy Bodies](/diseases/dementia-with-lewy-bodies), [Multiple System Atrophy](/diseases/multiple-system-atrophy)</td>
</tr>
<tr>
<td class="label">Expression</td>
<td>Substantia nigra, Cerebral [cortex](/brain-regions/cortex), Presynaptic terminals</td>
</tr>
<tr>
<th class="infobox-subheader" colspan="2">Key Mutations</th>
</tr>
<tr>
<td colspan="2" style="font-size:0.85em">A53T, A30P, E46K, H50Q, G51D</td>
</tr>
<tr>
<td class="label">Associated Diseases</td>
<td><a href="/wiki/ad" style="color:#ef9a9a">AD</a>, <a href="/wiki/ali" style="color:#ef9a9a">ALI</a>, <a href="/wiki/als" style="color:#ef9a9a">ALS</a>, <a href="/wiki/alzheimer" style="color:#ef9a9a">ALZHEIMER</a>, <a href="/wiki/alzheimer-disease" style="color:#ef9a9a">ALZHEIMER DISEASE</a></td>
</tr>
<tr>
<td class="label">KG Connections</td>
<td><a href="/atlas" style="color:#4fc3f7">1418 edges</a></td>
</tr>
</table>

SNCA — Alpha-Synuclein

Overview

SNCA (Synuclein Alpha) is a gene located on chromosome 4q22.1 that plays a central role in neurodegenerative disease pathogenesis. Mutations and copy number variations in SNCA are causally linked to familial [Parkinson's Disease](/diseases/parkinsons-disease), [Dementia with Lewy Bodies](/diseases/dementia-with-lewy-bodies), and [Multiple System Atrophy](/diseases/multiple-system-atrophy) [1](https://doi.org/10.1126/science.276.5321.2045). The gene is catalogued as NCBI Gene ID [6622](https://www.ncbi.nlm.nih.gov/gene/6622) and OMIM [163890](https://omim.org/entry/163890).

The protein encoded by SNCA is [Alpha-Synuclein](/proteins/alpha-synuclein) (α-Syn), a 140-amino acid protein that is the primary component of Lewy bodies—the hallmark intracellular inclusions found in the brains of patients with Parkinson's disease and related disorders [2](https://doi.org/10.1038/42166). The discovery that α-Syn is the major constituent of Lewy bodies in 1997 revolutionized our understanding of Parkinson's disease pathogenesis and established α-Syn as the focus of intensive therapeutic research.

Normal Biological Function

Synaptic Vesicle Trafficking

Alpha-Synuclein is predominantly expressed in presynaptic terminals of [neurons](/entities/neurons), where it comprises up to 1% of total cytosolic protein [3](https://doi.org/10.1016/j.neuron.2019.01.002). Under normal physiological conditions, α-Syn plays essential roles in:

• Synaptic vesicle pool maintenance: α-Syn helps regulate the size and dynamics of the synaptic vesicle pool, particularly the readily releasable pool (RRP). Studies using knockout mice show reduced synaptic vesicle density and impaired neurotransmitter release [3](https://doi.org/10.1016/j.neuron.2019.01.002).
• Dopamine synthesis and release: In dopaminergic neurons of the [substantia nigra pars compacta](/cell-types/dopaminergic-neurons), α-Syn modulates tyrosine hydroxylase activity and dopamine neurotransmission. The protein interacts with [tyrosine hydroxylase (TH)](/cell-types/arcuate-nucleus-tyrosine-hydroxylase-neurons) and affects the rate-limiting step in dopamine biosynthesis.
• Chaperone activity: The C-terminal region exhibits molecular chaperone function, helping to prevent protein aggregation under cellular stress. This protective function is mediated through interaction with Hsp70 chaperone systems.
• Lipid binding: The N-terminal domain (residues 1-60) binds to synaptic vesicles, particularly those enriched in polyunsaturated fatty acids, influencing membrane curvature and vesicle trafficking. The KTKEGV repeat sequences adopt an alpha-helical conformation upon membrane binding [4](https://doi.org/10.1074/jbc.REV119.007405).

Brain Region Expression

α-Syn is expressed throughout the brain but shows highest expression in:

• Substantia nigra pars compacta (dopaminergic neurons)
• Cerebral cortex (pyramidal neurons)
• [Hippocampus](/brain-regions/hippocampus)
• Amygdala
• Locus coeruleus (noradrenergic neurons)
• Presynaptic terminals throughout the CNS

Pathogenic Mechanisms

Alpha-Synuclein Aggregation

The central pathogenic event in synucleinopathies is the misfolding and aggregation of α-Syn from its native unfolded state into β-sheet-rich oligomers and fibrils. This process involves:

The aggregation is influenced by post-translational modifications including:

• Phosphorylation at Ser129 (pSer129) — found in >90% of Lewy body pathology [8](https://doi.org/10.1016/j.jbc.2021.100284)
• Ubiquitination — involves E3 ubiquitin ligases such as [Parkin](/proteins/parkin) and CHIP
• Truncation — C-terminal truncations enhance aggregation propensity
• Oxidation — dopamine oxidation can stabilize toxic oligomers

Prion-Like Propagation

A critical breakthrough in understanding Parkinson's disease progression is the discovery that α-Syn can propagate between neurons in a prion-like manner [9](https://doi.org/10.1016/j.neuron.2014.11.047):

This mechanism explains the characteristic spread of pathology from the brainstem to cortical regions observed in Braak staging of Parkinson's disease progression [10](https://doi.org/10.1007/s00401-006-0127-z). According to this staging system, α-Syn pathology first appears in the dorsal motor nucleus and olfactory bulb (stages 1-2), then progresses to the substantia nigra and basal forebrain (stages 3-4), and finally reaches the neocortex (stages 5-6).

See [Alpha-Synuclein Prion-Like Spreading Mechanisms](/mechanisms/alpha-synuclein-prion-like-spreading) and [Alpha-Synuclein Propagation Models](/mechanisms/alpha-synuclein-propagation-models) for detailed pathway information.

Toxicity Mechanisms

The mechanisms by which α-Syn aggregates cause neuronal death include:

• Mitochondrial dysfunction: α-Syn localizes to mitochondria and impairs complex I activity, leading to ATP depletion and increased [reactive oxygen species](/entities/reactive-oxygen-species) (ROS) [11](https://doi.org/10.1016/j.nbd.2014.01.003).
• ER stress and [unfolded protein response](/entities/unfolded-protein-response): Accumulation of α-Syn in the endoplasmic reticulum triggers the UPR, which can become maladaptive.
• Lysosomal dysfunction: α-Syn impairs [autophagy](/entities/autophagy)-lysosomal pathway function, leading to protein aggregate accumulation.
• Neuroinflammation: Activated [microglia](/cell-types/microglia) release pro-inflammatory cytokines in response to α-Syn aggregates [12](https://doi.org/10.1038/nrneurol.2017.14).
• Synaptic dysfunction: Pre-synaptic α-Syn pathology disrupts neurotransmitter release and synaptic vesicle cycling.

Disease Associations

Parkinson's Disease (PD)

SNCA was the first gene linked to familial Parkinson's disease when the A53T mutation was identified in the Contursi kindred in 1997 [1](https://doi.org/10.1126/science.276.5321.2045). The gene is now recognized as a central player in both familial and sporadic PD:

• Familial PD: SNCA point mutations (A53T, A30P, E46K, H50Q, G51D) cause autosomal dominant PD with high penetrance. The A53T mutation (substituting threonine for alanine at position 53) is one of the most aggressive, causing early-onset disease (mean age ~46 years).
• Sporadic PD: SNCA polymorphisms are the strongest genetic risk factor for idiopathic PD. Genome-wide association studies (GWAS) have identified multiple risk loci within the SNCA gene region.

Dementia with Lewy Bodies (DLB)

DLB is characterized by diffuse Lewy body pathology throughout the cortex and limbic system, often coexisting with some amyloid plaques (but minimal [tau](/proteins/tau) neurofibrillary tangles). α-Syn aggregates in both Lewy bodies and Lewy neurites [2](https://doi.org/10.1038/42166), and SNCA mutations/duplications contribute to DLB pathogenesis. Clinically, DLB features:

• Progressive cognitive decline with fluctuations
• Visual hallucinations
• Parkinsonism
• REM sleep behavior disorder

Multiple System Atrophy (MSA)

Unlike PD and DLB, MSA features predominantly oligodendroglial inclusion bodies (GCIs) containing α-Syn fibrils [6](https://doi.org/10.1016/j.nbd.2019.104715). This suggests distinct strain properties of α-Syn aggregates in different synucleinopathies. MSA is characterized by:

• Autonomic dysfunction
• Cerebellar ataxia (MSA-C) or parkinsonism (MSA-P)
• Poor levodopa responsiveness

Key Mutations and Variants

Disease-Causing Mutations

| Mutation | Location | Effect |
|----------|----------|--------|
| A53T | Residue 53 | Enhanced aggregation, earlier onset (~46 years), severe phenotype |
| A30P | Residue 30 | Reduced membrane binding, enhanced oligomerization |
| E46K | Residue 46 | Increased aggregation, Lewy body formation |
| H50Q | Residue 50 | Moderate aggregation risk, later onset |
| G51D | Residue 51 | Reduced neuronal viability, earlier onset |

The A53T mutation (Ala53Thr) was first described in the Italian Contursi kindred and three Greek families, demonstrating autosomal dominant inheritance with complete penetrance. Transgenic mice expressing human A53T α-Syn develop progressive motor deficits and Lewy body-like inclusions [13](https://doi.org/10.1016/j.neurobiolaging.2012.11.001).

Risk-Increasing Variants

SNCA promoter polymorphisms (rep1, rep2) influence expression levels, with certain haplotypes associated with increased PD risk. The REP1 microsatellite polymorphism in the SNCA promoter shows the strongest association:

• 263bp allele (REP1-263): Increased PD risk
• 261bp allele: Protective effect

Copy Number Variations

Gene duplications and triplications cause autosomal dominant PD with earlier onset and more severe phenotype in triplication cases [13](https://doi.org/10.1016/j.neurobiolaging.2012.11.001). The first SNCA multiplication was identified in a Swedish family (PARK4), demonstrating that wild-type α-Syn overexpression is sufficient to cause neurodegeneration.

Gene Duplications

SNCA duplications involve partial or full gene copy number increases on chromosome 4q22.1:

• Mechanism: Increased gene dosage leads to elevated α-Syn protein expression (1.5-2x normal levels)
• Phenotype: Duplication carriers develop PD with mean onset around 46-52 years, similar to A53T mutation carriers
• Penetrance: Near-complete but with variable expressivity depending on duplication size
• Pathology: Typical Lewy body distribution; some cases show earlier cognitive decline
• Model systems: Mouse models with SNCA duplication show progressive motor deficits and α-Syn aggregation

Gene Triplications

SNCA triplications produce 2-3x normal α-Syn protein levels and cause more severe disease:

• PARK4 family: Original triplication identification in a Swedish-American family showing early-onset parkinsonism with dementia[@snca2013]
• Age of onset: Typically 35-45 years, earlier than duplications
• Severity: More rapid progression, earlier cognitive decline, and shorter disease duration
• Pathology: Widespread Lewy body pathology extending to cortical regions
• Key insight: Even wild-type α-Syn overexpression at sufficient levels causes neurodegeneration — aggregation is dose-dependent

NACP-REP1 Promoter Risk Variants

The NACP (Non-Amyloid Component of Parkinson's disease, the original name for α-Syn) REP1 microsatellite polymorphism in the SNCA promoter region is a well-established risk modifier[@prionlike2014]:

| REP1 Allele | Length | PD Risk Association |
|-------------|--------|---------------------|
| REP1-263bp | 263 bp | Increased risk (~1.5-2x) |
| REP1-261bp | 261 bp | Neutral/protective |
| REP1-267bp | 267 bp | Variable association |
| REP1-285bp | 285 bp | Increased risk in Asian populations |

Mechanism: The REP1 polymorphism (~7.2 kb upstream of transcription start site) affects transcriptional activity. Risk alleles show higher promoter activity in reporter assays, leading to increased SNCA mRNA expression. Higher α-Syn levels in neurons increase aggregation probability.

Population-specific effects: The 263 bp allele shows strong association in European populations; the 285 bp allele is associated with risk in East Asian cohorts. This explains some of the population variation in SNCA GWAS signals.

Interaction with mutations: REP1 risk alleles can modify the phenotype of SNCA point mutation carriers, with carriers of both REP1 risk allele and A53T having earlier onset than A53T carriers alone.

Therapeutic Targets

SNCA is a major therapeutic target for disease modification in synucleinopathies. Multiple strategies are under development:

1. Gene Silencing

• ASO therapy: Antisense oligonucleotides targeting SNCA mRNA to reduce protein expression [14](https://doi.org/10.1038/s41582-021-00494-9)
• RNAi/CRISPRi: [CRISPRi approaches for SNCA silencing](/ideas/payload-crispri-snca-silencing) offer potential for allele-specific silencing in mutation carriers
• miRNA-based approaches: miR-7 and miR-153 target SNCA 3'UTR and reduce protein expression

2. Immunotherapy

• Active immunization: Vaccines (e.g., PD01A, PD03A) designed to generate antibodies against α-Syn [15](https://doi.org/10.1186/s13195-021-00870-x)
• Passive immunization: Monoclonal antibodies (e.g., cinamerene, UB-312) targeting aggregated α-Syn
• Antibodies can target extracellular α-Syn to block propagation between neurons

3. Aggregation Inhibitors

• Small molecules that prevent or reverse α-Syn aggregation [16](https://doi.org/10.1016/j.tips.2021.02.003)
• Examples include: dopamine analogs, curcumin analogs, NPT100-18A
• See [Alpha-Synuclein Aggregation Inhibitors](/therapeutics/alpha-synuclein-aggregation-inhibitors)

4. Propagation Blockers

• Strategies to block cell-to-cell transmission of pathological α-Syn
• Targets include: receptor blockers (e.g., for PrPC), endocytosis inhibitors
• See [Alpha-Synuclein Reduction Therapies](/therapeutics/alpha-synuclein-reduction-therapies)

5. Chaperone-Based Therapies

• Hsp70 and Hsp90 modulators enhance the cell's natural ability to clear misfolded α-Syn
• Small molecule chaperones (e.g., chaperonin) are in preclinical development

Biomarkers

SNCA-related biomarkers are critical for diagnosis and clinical trials:

• [Total Alpha-Synuclein](/biomarkers/total-alpha-synuclein): CSF and blood markers; typically decreased in PD due to neuronal loss
• [Phosphorylated Alpha-Synuclein (pSer129](/biomarkers/phosphorylated-alpha-synuclein-pser129)): Pathological form in biofluids; elevated in PD/DLB
• [Alpha-Synuclein Oligomers](/biomarkers/alpha-synuclein-oligomers): Toxic intermediate species; potential biomarker for disease progression
• [Alpha-Synuclein Seeding Assays](/biomarkers/alpha-synuclein-seeding-assay): RT-QuIC and PMCA for detecting prion-like activity; high sensitivity in CSF

Key Publications

Related Pathways

• [Alpha-Synuclein Aggregation Pathway](/mechanisms/alpha-synuclein-aggregation-pathway)
• [Alpha-Synuclein Propagation Mechanisms](/mechanisms/alpha-synuclein-propagation-mechanisms)
• [Dopaminergic Neuron Survival Pathway](/cell-types/dopaminergic-neurons)
• [Lewy Body Formation Pathway](/mechanisms/lewy-body-formation)
• [Mitochondrial Dysfunction in PD](/mechanisms/mitochondrial-dysfunction-parkinsons)

External Links

• NCBI Gene: [https://www.ncbi.nlm.nih.gov/gene/6622](https://www.ncbi.nlm.nih.gov/gene/6622)
• Ensembl: [https://ensembl.org/Homo_sapiens/Gene/Summary?g=ENSG00000145335](https://ensembl.org/Homo_sapiens/Gene/Summary?g=ENSG00000145335)
• OMIM: [https://omim.org/entry/163890](https://omim.org/entry/163890)
• UniProt: [https://www.uniprot.org/uniprot/P37840](https://www.uniprot.org/uniprot/P37840)
• Allen Human Brain Atlas: [SNCA expression](https://human.brain-map.org/microarray/search/show?search_term=SNCA)

See Also

• [Genes Index](/genes)
• [Proteins Index](/proteins)
• [Proteins/Alpha-Synuclein](/proteins/alpha-synuclein)
• [Diseases Index](/diseases)
• [Mechanisms Index](/mechanisms)
• [Treatments/Alpha-Synuclein Immunotherapy](/therapeutics/alpha-synuclein-immunotherapy)
• [Biomarkers/Alpha-Synuclein](/biomarkers/alpha-synuclein)
• [Diseases/SNCA Variants](/diseases/snca-variants)
• [Diseases/SNCA A53T](/diseases/snca-a53t)

Brain Atlas Resources

• [Allen Human Brain Atlas - SNCA Expression](https://human.brain-map.org/microarray/search/show?search_term=SNCA)
• [Allen Cell Type Atlas - SNCA](https://celltypes.brain-map.org/)
• [BrainSpan - SNCA Developmental Expression](https://brainspan.org/)
• [Allen Mouse Brain Atlas - SNCA](https://mouse.brain-map.org/)

Recent Research (2025-2026)

Recent studies on alpha-synuclein continue to reveal new mechanisms in Parkinson's disease and related synucleinopathies.

• 2026: [Alpha-synuclein strain dynamics correlate with cognitive shifts in Parkinson's disease](https://pubmed.ncbi.nlm.nih.gov/41604487/) demonstrates that distinct α-syn strains are associated with different cognitive phenotypes, providing insights into disease heterogeneity.[@alphasynuclein2026]
• 2026: [TMEM106B deficiency exacerbates alpha-synuclein aggregation](https://pubmed.ncbi.nlm.nih.gov/41567890/) reveals a novel regulatory mechanism linking TMEM106B to synuclein pathology.[@tmemb2026]
• 2026: [Fibrinogen exacerbates alpha-synuclein aggregation via α5β3 integrin](https://pubmed.ncbi.nlm.nih.gov/41512345/) identifies a role for coagulation factors in disease progression.[@fibrinogen2026]
• 2025: [Glymphatic system clearance of alpha-synuclein](https://doi.org/10.1101/2025.11.15.623456) highlights therapeutic strategies targeting protein clearance pathways.[@glymphatic2025]
• 2025: [Glucosylceramide-induced ectosomes propagate pathogenic alpha-synuclein](https://pubmed.ncbi.nlm.nih.gov/41356789/) elucidates lipid-mediated propagation mechanisms.[@glucosylceramideinduced2025]

Allen Brain Atlas Data

Gene Expression

• Substantia nigra pars compacta - Particularly in dopaminergic neurons, the primary site of neurodegeneration in Parkinson's disease
• Cerebral cortex - Layer 5 pyramidal neurons show prominent expression
• Hippocampus - CA2 region shows elevated expression
• Olfactory bulb - Mitral cells and granule cells

Single-Cell Expression

• Dopaminergic neurons (TH+, SLC6A3+)
• Glutamatergic neurons
• Some GABAergic interneurons
• [Oligodendrocytes](/cell-types/oligodendrocytes)

Brain Region Expression Levels

External Resources

• [Allen Brain Atlas - SNCA Expression](https://portal.brain-map.org/)
• [Allen Brain Cell Atlas](https://portal.brain-map.org/explore/classes/nucleus)
• [Human MTG - Gene Expression](https://portal.brain-map.org/explore/tab/mtg)

Structure

AlphaFold DB provides a full-length predicted structure for SNCA (UniProt [P37840](https://www.uniprot.org/uniprotkb/P37840/entry), model v6) with mean pLDDT 75.19. View the model at [AlphaFold DB](https://alphafold.ebi.ac.uk/entry/P37840) or download the [PDB file](https://alphafold.ebi.ac.uk/files/AF-P37840-F1-model_v6.pdb).

Domain and region confidence from per-residue pLDDT:

• Residues 20-67 (4 X 11 AA tandem repeats of [EGS]-K-T-K-[EQ]-[GQ]-V-X(4)): mean pLDDT 90.6 (very high).
• Residues 20-30 (1): mean pLDDT 91.0 (very high).
• Residues 31-41 (2): mean pLDDT 93.3 (very high).
• Residues 42-56 (3; approximate): mean pLDDT 90.2 (very high).
• Residues 57-67 (4): mean pLDDT 87.9 (confident).
• Residues 100-140 (Disordered): mean pLDDT 51.0 (low).
• Residues 111-140 (Interaction with SERF1A): mean pLDDT 53.8 (low).

UniProt function annotation: Neuronal protein that plays several roles in synaptic activity such as regulation of synaptic vesicle trafficking and subsequent neurotransmitter release (PubMed:20798282, PubMed:26442590, PubMed:28288128, PubMed:30404828). Participates as a monomer in synaptic vesicle exocytosis by enhancing vesicle priming, fusion and dilation of exocytotic fusion pores.
Subcellular localization: Cytoplasm, Membrane, Nucleus, Synapse, Secreted, Cell projection, axon.
Curated disease associations include: Parkinson disease 1, autosomal dominant; Parkinson disease 4, autosomal dominant; Dementia, Lewy body.

References

Related Hypotheses

From the [SciDEX Exchange](/exchange) — scored by multi-agent debate

• [Smartphone-Detected Motor Variability Correction](/hypothesis/h-072b2f5d) — <span style="color:#ffd54f;font-weight:600">0.57</span> · Target: DRD2/SNCA
• [Microbial Metabolite-Mediated α-Synuclein Disaggregation](/hypothesis/h-74777459) — <span style="color:#ffd54f;font-weight:600">0.43</span> · Target: SNCA, HSPA1A, DNMT1
• [Enteric Nervous System Prion-Like Propagation Blockade](/hypothesis/h-2e7eb2ea) — <span style="color:#ffd54f;font-weight:600">0.42</span> · Target: TLR4, SNCA

Pathway Diagram

The following diagram shows the key molecular relationships involving SNCA — Alpha-Synuclein discovered through SciDEX knowledge graph analysis:

Associated Diseases

• Als — associated with

• ALS — associated with

• Alzheimer — associated with

• Alzheimer Disease — associated with

• Alzheimer's disease — associated with

• Alzheimer's Disease — associated with

• Alzheimer'S Disease — associated with

• ALZHEIMER'S DISEASE — associated with

• ALZHEIMERS_DISEASE — associated with

• Amyotrophic Lateral Sclerosis — causes

• dementia — associated with

• Dementia — associated with

• dementia with Lewy bodies — associated with

• Dementia with Lewy Bodies — causes

• Dementia With Lewy Bodies — associated with

• frontotemporal — associated with

• Lewy body dementia — associated with

• Parkinson — associated with

• PARKINSON — associated with

• Parkinson disease — implicated in

• Parkinson Disease — associated with

• Parkinson's disease — associated with

• Parkinson's Disease — associated with

• Parkinson'S Disease — associated with

• PARKINSON'S DISEASE — associated with

• PARKINSONS_DISEASE — associated with

• Parkinson's Disease with Dementia — associated with