"Which AD, PD, ALS, and FTD mechanisms recur across disease boundaries and yield falsifiable experiments?"
Comparing top 3 hypotheses across 8 scoring dimensions
Multi-agent debate between AI personas, each bringing a distinct perspective to evaluate the research question.
Generates novel, bold hypotheses by connecting ideas across disciplines
Mechanism: Impaired autophagic flux and lysosomal degradation capacity represents a convergent failure point across AD, PD, ALS, and FTD, leading to accumulation of toxic protein species (tau, α-synucl
...Mechanism: Impaired autophagic flux and lysosomal degradation capacity represents a convergent failure point across AD, PD, ALS, and FTD, leading to accumulation of toxic protein species (tau, α-synuclein, TDP-43, SOD1).
Target Gene/Protein/Pathway:
| Disease | Evidence | PMIDs |
|--------|----------|-------|
| AD | TFEB overexpression reduces tau and Aβ pathology in 3xTg mice; mTOR hyperactivation impairs autophagy in AD brain | 26507055, 22879586 |
| PD | TMEM175 loss-of-function variants increase PD risk (GWAS); GBA1 mutations → 20x PD risk via lysosomal dysfunction | 29446782, 25296885 |
| ALS/FTD | ALS-linked CHMP2B mutations impair autophagosome-lysosome fusion; TDP-43 aggregation disrupts autophagy initiation | 17689134, 23811925 |
| Cross-disease | Declining lysosomal enzyme activity documented across NDDs in human postmortem tissue | 29977472 |
Predicted Experiment:
Confidence: 0.82
Mechanism: TDP-43 misfolding, cytoplasmic aggregation, and loss of nuclear function occurs as a primary or secondary pathology across all four diseases, representing a convergent downstream effect of diverse upstream stressors (RNA toxicity, proteostatic overload, phosphorylation stress).
Target Gene/Protein/Pathway:
| Disease | Evidence | PMIDs |
|--------|----------|-------|
| ALS/FTD | TDP-43 inclusions are the defining pathology (~95% ALS, ~50% FTD); 50+ TARDBP mutations identified | 17077305, 18539960 |
| AD | Limbic-predominant age-related TDP-43 neuropathologic change (LATE-ND) in 20-50% of AD cases; associates with faster cognitive decline | 31138799, 31321539 |
| PD | TDP-43 pathology in 10-15% of PD cases, associated with dementia phenotype | 19251658, 24521246 |
Predicted Experiment:
Confidence: 0.79
Mechanism: Disease-specific protein aggregates (Aβ, α-synuclein, TDP-43) activate microglia via pattern recognition receptors (TLRs, NLRP3), driving chronic neuroinflammation that amplifies neuronal loss independent of the initial disease trigger.
Target Gene/Protein/Pathway:
| Disease | Evidence | PMIDs |
|--------|----------|-------|
| AD | TREM2 R47H variant (3x AD risk); Trem2 deletion impairs Aβ microglial containment in 5xFAD mice; NLRP3KO protects against Aβ pathology | 25480569, 26237648, 24154525 |
| PD | NLRP3 activation by α-synuclein fibrils; CX3CR1 KO increases MPTP toxicity; GBA1 loss activates microglia via inflammasome | 26824394, 22506280 |
| ALS/FTD | TDP-43 aggregates activate NLRP3; C9orf72 loss drives spontaneous microglial activation; C1q deposition on motor neurons | 30970244, 31270427 |
| Cross-disease | Single-cell RNA-seq reveals shared MGnD transcriptional signature across AD, PD, ALS mouse models | 31413159 |
Predicted Experiment:
Confidence: 0.85
Mechanism: Impaired RNA processing and disrupted nucleocytoplasmic transport represent a convergent molecular phenotype across AD, PD, ALS, and FTD, arising from distinct genetic causes but converging on common downstream consequences for protein homeostasis and stress response.
Target Gene/Protein/Pathway:
| Disease | Evidence | PMIDs |
|--------|----------|-------|
| ALS/FTD | C9orf72 hexanucleotide expansion (~10% ALS, ~25% FTD) causes RAN translation, DPR toxicity, and NCT disruption; RanGAP1 mislocalization in C9orf72 iNs | 25527282, 28132797 |
| AD | Nuclear pore deterioration in AD brain (electron microscopy); NUP205 expression correlates with cognitive decline; TDP-43 loss disrupts NTF transport | 28202704, 30106399 |
| PD | RNA-seq in PD substantia nigra reveals splicing defects; LRRK2 G2019S associates with altered RNA splicing | 27782121, 25500530 |
| Cross-disease | Genome-wide association studies link NCT genes to ALS, PD, and AD risk | 28714951, 30745317 |
Predicted Experiment:
Confidence: 0.72
Mechanism: Impaired mitochondrial dynamics (fission/fusion), reduced mitophagy, and accumulated mitochondrial DNA mutations represent a shared energy crisis across neurodegeneration, converging on synaptic vulnerability and neuronal death.
Target Gene/Protein/Pathway:
| Disease | Evidence | PMIDs |
|--------|----------|-------|
| PD | PINK1/PARKIN mutations cause early-onset familial PD; PINK1 KO in mice causes mitochondrial dysfunction and dopamine neuron loss | 16148542, 15731009 |
| AD | mtDNA mutations accumulate in AD brain; DRP1 hyperactivation causes mitochondrial fragmentation; PINK1 reduction in AD cortex | 26928465, 24997960 |
| ALS | TDP-43 loss of function impairs mitochondrial transport; CHCHD10 mutations cause ALS/FTD; mutant SOD1 disrupts mitochondrial import | 26586676, 23851801 |
| Cross-disease | Reduced NAD+ levels documented across NDD models; NR supplementation improves outcomes in ALS, AD, and PD models | 27832538, 28720827 |
Predicted Experiment:
Confidence: 0.77
Mechanism: Disrupted retrieval of cargo from endosomes to the trans-Golgi network (retromer dysfunction) leads to impaired processing of amyloid precursor protein (APP), α-synuclein trafficking, and TDP-43 clearance, representing a shared vesicle trafficking defect.
Target Gene/Protein/Pathway:
| Disease | Evidence | PMIDs |
|--------|----------|-------|
| AD | SORL1 variants increase AD risk; VPS26 SNP associated with AD; retromer protein levels reduced in AD brain; VPS35 overexpression reduces Aβ in mouse models | 19103625, 21908926, 22106805 |
| PD | VPS35 D620N mutation causes late-onset familial PD; leads to impaired retromer function and altered autophagy; links to α-synuclein trafficking | 23077058, 23811924 |
| ALS/FTD | Retromer complex subunits downregulated in ALS spinal cord; CHMP2B (ESCRT-III) mutations cause FTD; VPS35 reduction impairs lysosomal proteostasis | 17689134, 26928465 |
| Cross-disease | Genetic variants in retromer components identified across NDD GWAS; functional convergence on lysosomal trafficking | 21908926, 28714951 |
Predicted Experiment:
Confidence: 0.74
Mechanism: Impaired brain insulin/IGF-1 signaling and reduced glucose metabolism represent a shared metabolic failure across AD, PD, ALS, and FTD, contributing to energy deficits, impaired protein clearance, and synaptic dysfunction through convergent AKT/mTOR pathway dysregulation.
Target Gene/Protein/Pathway:
| Disease | Evidence | PMIDs |
|--------|----------|-------|
| AD | "Type 3 Diabetes" hypothesis; IRS1 phosphorylation increased in AD brain; reduced INSR/IGF1R expression; intranasal insulin improves memory | 27882449, 26449472 |
| PD | IRS2 knockout protects against MPTP in PD mice; IGF-1 rescues α-synuclein toxicity; diabetes increases PD risk | 27782121, 21956373 |
| ALS | ALS cerebrospinal fluid inhibits neuronal insulin signaling in vitro; IGF-1 trials (negative); metabolic dysregulation evident in ALS metabolomics | 27426923, 28327495 |
| FTD | TREM2 risk allele in FTD-AD continuum; brain insulin resistance in FTD (preliminary
Challenges assumptions, identifies weaknesses, and provides counter-evidence
| Finding | Source | Implication |
|---------|--------|-------------|
| Selective autophagy knockouts rarely cause spontaneous NDD | Multiple conditional KO models (Atg5, Atg7 neuronal KO) produce neurodegeneration but not disease-specific proteinopathies | General autophagy impairment may not explain disease specificity |
| TMEM175 GWAS effect size modest | Odds ratio ~1.4-1.6 for PD risk variants | Likely a modifier rather than core mechanism; most PD patients lack this variant |
| Lysosomal enzyme declines are late findings | Postmortem tissue reflects end-stage disease | Cannot distinguish cause from consequence |
The mechanistic pathway is plausible but insufficiently validated as a primary driver vs. disease amplifier. The hypothesis generates more falsifiable predictions than most, but current evidence is predominantly correlative. Strong evidence of TFEB sufficiency in mice does not establish necessity in human disease.
| Finding | Source | Implication |
|---------|--------|-------------|
| TARDBP mutations do not cause AD/PD | No reported TARDBP mutations in familial AD or PD cohorts | TDP-43 dysfunction is unlikely to be upstream cause in non-ALS/FTD diseases |
| TDP-43 pathology often localizes to regions affected by primary disease |尸检 studies show TDP-43 in limbic system in LATE-ND vs. motor neurons in ALS | Spreading may be downstream, not convergent upstream |
| TDP-43 KO mice develop subtle phenotypes | Conditional KO models show mild phenotypes compared to disease models | TDP-43 loss alone is insufficient to explain neurodegeneration severity |
The hypothesis conflates primary pathology (ALS/FTD) with secondary involvement (AD/PD). The proposed experiments are well-designed but would primarily confirm secondary roles rather than establish unifying causation. TDP-43 may be better characterized as a disease-specific substrate whose aggregation is sometimes cross-seeded, not a convergent mechanism.
| Finding | Source | Implication |
|---------|--------|-------------|
| MCC950 (NLRP3 inhibitor) failed in clinical trials | Phase II trials for inflammatory diseases showed limited efficacy and toxicity | Strongest human relevance evidence is negative |
| Anti-inflammatory interventions don't prevent NDDs | Large NSAID prevention trials (e.g., ADAPT) showed no benefit | Supports neuroinflammation as downstream effect |
| TREM2 KO in 5xFAD has mixed phenotype | Some studies show worsening, others show protective effects depending on timing | Context-dependence undermines therapeutic potential |
| CX3CR1 KO studies inconsistent | Different toxins and timing produce conflicting results | Species/strain differences confound interpretation |
Despite the highest initial confidence, this hypothesis has the poorest clinical translation record. The proposed experiments are sound but would need to overcome a substantial burden of negative evidence. Confidence was likely inflated by animal model evidence that consistently fails to translate.
| Finding | Source | Implication |
|---------|--------|-------------|
| RanGAP1 mislocalization is C9orf72-specific | iPSC studies show this primarily in C9orf72 lines | May not generalize to other diseases |
| AD nuclear pore deterioration is late-stage | EM findings often describe end-stage pathology | Insufficient to explain early cognitive impairment |
| RNA splicing defects are ubiquitous in neurodegeneration | Splicing abnormalities appear in virtually all NDDs | May be a general distress signal, not disease-specific |
This hypothesis has the weakest cross-disease evidence of those presented. The core mechanism is well-established for C9orf72 ALS/FTD, but extension to AD and PD is speculative. Confidence was likely inflated by the compelling C9orf72 biology.
| Finding | Source | Implication |
|---------|--------|-------------|
| PINK1 KO mice have limited neurodegeneration | Spontaneous phenotypes require aging or stressors | Pink1 loss alone is insufficient |
| No PINK1/Parkin mutations in ALS/FTD/AD | Familial ALS, FTD, and AD cohorts lack PINK1/Parkin variants | Mechanism may be disease-specific |
| Mitophagy reporters show baseline dysfunction | Normal aging includes declining mitophagy | May be age-related, not disease-specific |
Assesses druggability, clinical feasibility, and commercial viability
Bottom Line
Most feasible near-term development paths are not “one drug for AD/PD/ALS/FTD.” The tractable version is mechanism-stratified development: use cross-disease biology to nominate biomarkers and patient subsets, then run disease-specific or genetically enriched trials.
My feasibility ranking:
Bottom Line
Most feasible near-term development paths are not “one drug for AD/PD/ALS/FTD.” The tractable version is mechanism-stratified development: use cross-disease biology to nominate biomarkers and patient subsets, then run disease-specific or genetically enriched trials.
My feasibility ranking:
1. Autophagy-Lysosomal Dysfunction
Feasibility: moderate-high as a platform; moderate as a drug program.
Druggability is plausible but not simple. TFEB activation is attractive, but direct systemic TFEB activation risks broad effects on metabolism, immunity, lysosomal expansion, and possibly tumor biology. Better druggable entry points are GBA1 enhancement, TMEM175 modulation, retromer stabilization, mTOR-independent lysosomal activation, or brain-targeted gene therapy in rare genetic subsets.
Best biomarkers: CSF/plasma lysosomal enzymes, GCase activity, cathepsins, LAMP1/2, LC3-II/p62 in cells, PET if lysosomal tracers mature, plus proteinopathy-specific readouts: tau PET, α-syn SAA, NfL. iPSC neurons/macrophage-microglia co-cultures and aged knock-in models are preferable to aggressive overexpression mice.
Clinical constraint: broad sporadic AD/PD/ALS trials would be expensive and underpowered unless enriched by GBA1, TMEM175, VPS35, lysosomal biomarker-low patients. A first proof-of-biology trial in GBA1-PD or prodromal GBA1 carriers is more realistic.
Safety: chronic lysosomal upregulation could disturb immune function, lipid handling, and neuronal homeostasis. AAV-TFEB is not first-line clinically because dosing, reversibility, and long-term CNS safety are major barriers.
Timeline/cost: biomarker-enriched Phase 1b/2a small molecule: 4-6 years, $40-90M. Gene therapy route: 7-10+ years, $150-300M+.
2. TDP-43 Proteinopathy
Feasibility: high for ALS/FTD precision development; low as pan-AD/PD therapy.
The strongest investable version is not “TDP-43 across all neurodegeneration,” but TDP-43-positive ALS/FTD and LATE/AD subgroups. TDP-43 is hard to drug directly, but ASOs, RNA/splicing rescue, aggregation blockers, nuclear localization stabilizers, and stress-granule modulators are plausible. The tofersen precedent matters: FDA accelerated approval for SOD1-ALS was based on NfL reduction, showing that genetically defined ALS can use biomarker-driven development ([Biogen/FDA release](https://investors.biogen.com/news-releases/news-release-details/fda-grants-accelerated-approval-qalsodytm-tofersen-sod1-als)).
Best biomarkers: TDP-43 seed amplification assays are becoming more credible; a 2025 study detected CSF TDP-43 seeding in symptomatic and some presymptomatic genetic FTD/ALS carriers, with reported 67% sensitivity in TDP-43-linked symptomatic patients and 93% specificity ([PubMed](https://pubmed.ncbi.nlm.nih.gov/41399249/)). Also use cryptic-exon/splicing biomarkers, NfL, pNfH, MRI atrophy, EMG/ALSFRS-R for ALS, and CDR/FTD scales for dementia.
Model systems: C9orf72, GRN, TARDBP, UBQLN2 iPSC neurons and assembloids are useful; overexpression TDP-43 mice are often toxic artifacts. Human pathology-anchored models are essential.
Clinical constraint: AD/PD inclusion only makes sense if patients are biomarker-positive for TDP-43. Otherwise effect dilution is fatal.
Safety: lowering or altering TDP-43 is dangerous because nuclear TDP-43 has essential RNA-processing functions. Therapeutics must avoid excessive knockdown.
Timeline/cost: ALS/FTD biomarker-positive Phase 1b/2a: 3-5 years, $50-120M. AD/LATE subgroup program: 6-9 years, $150-400M, mostly due to diagnosis and endpoint burden.
3. Microglial Neuroinflammation / NLRP3 / TREM2
Feasibility: moderate biologically, low-moderate clinically.
This is real disease biology, but the clinical translation risk is high. The strongest caution is TREM2: AL002 showed target engagement and microglial pharmacodynamics but failed Phase 2 clinical and biomarker efficacy in early AD ([Alector 2024 results](https://investors.alector.com/news-releases/news-release-details/alector-announces-results-al002-invoke-2-phase-2-trial/)); the randomized trial has since been published in 2026 ([Nature Medicine](https://www.nature.com/articles/s41591-026-04273-1)). That does not kill microglial biology, but it weakens simple “activate TREM2” development.
Druggability: NLRP3 is druggable chemically; TREM2 is antibody-druggable; complement is druggable. But CNS exposure, cell-state specificity, and timing are the core problems. MCC950 is useful experimentally, not a clean development candidate.
Best biomarkers: TSPO PET is noisy; better panels include sTREM2, YKL-40, GFAP, IL-1β/IL-18 where measurable, complement fragments, ASC specks, snRNA-seq state signatures, amyloid/tau/α-syn/TDP-43 disease markers, and NfL.
Model systems: human iPSC microglia-neuron-astrocyte co-cultures, xenotransplanted human microglia mice, aged knock-in disease models. Standard young transgenic mice overpredict efficacy.
Clinical constraint: likely needs disease-stage selection. Early inflammation may be protective; late inflammation may be harmful. A flat inhibitor/agonist across all stages is risky.
Safety: immunosuppression, infection risk, impaired debris clearance, amyloid-related imaging changes for some immune-activating approaches, systemic inflammasome liabilities.
Timeline/cost: repurposed/known CNS-penetrant anti-inflammatory biomarker trial: 3-5 years, $30-80M. Novel CNS microglial drug to Phase 2: 6-9 years, $120-300M.
4. RNA Metabolism / Nucleocytoplasmic Transport
Feasibility: high in C9orf72 ALS/FTD; low as cross-disease AD/PD program.
Druggability is strongest through ASOs, RNA-targeting small molecules, DPR-lowering strategies, nuclear import/export modifiers, and stress granule biology. For AD/PD, the biology is currently too nonspecific.
Best biomarkers: DPR proteins in CSF for C9orf72, poly(GP), NfL, cryptic exon markers, nuclear/cytoplasmic RanGAP1/NUP localization in patient cells, RNA-seq splicing signatures. For AD/PD there is no validated clinical NCT biomarker.
Model systems: C9orf72 iPSC motor neurons/cortical neurons and organoids are appropriate. For AD/PD, use models only as secondary validation after showing patient-cell nuclear transport defects.
Clinical constraint: feasible trial population is C9orf72 carriers, including presymptomatic or early symptomatic cohorts. Cross-disease trials are premature.
Safety: broad nuclear transport modulation is high-risk because it touches essential cell biology. ASOs against specific toxic transcripts are safer conceptually.
Timeline/cost: C9orf72-focused ASO/small molecule program: 4-7 years, $80-200M. Pan-NDD NCT program: not trial-ready.
5. Mitochondrial Quality Control / NAD+
Feasibility: moderate-high for early trials; low as disease-modifying claim.
This is the easiest to test clinically because NAD+ boosters and metabolic interventions have tolerability precedent. The NADPARK Phase 1 PD trial reported oral nicotinamide riboside increased brain NAD and was safe over 30 days ([Cell Metabolism](https://www.sciencedirect.com/science/article/pii/S1550413122000456)). But “mitochondrial dysfunction” is broad aging biology, so a positive biomarker effect may not translate into slowed neurodegeneration.
Druggability: NAD+ supplementation, AMPK/SIRT modulation, mitophagy enhancers, PINK1/Parkin activators, mitochondrial-targeted antioxidants. PINK1/Parkin is genetically strong in PD but not cross-disease.
Best biomarkers: 31P-MRS brain NAD, CSF/plasma NAD metabolites, lactate/pyruvate, acylcarnitines, mitochondrial DNA damage, NfL, disease-specific progression markers. Need target engagement plus neurodegeneration markers.
Model systems: mito-QC mice are useful for flux, but human iPSC neurons with stress paradigms are better for translatability. Avoid relying on toxin models alone.
Clinical constraint: good for Phase 2 biomarker trials in PD or mild AD, but pivotal disease-modification trials would be large and expensive unless enriched by mitochondrial biomarker deficits.
Safety: NR/NMN generally manageable, but long-term effects on cancer biology, methyl donor balance, liver metabolism, and immune state need monitoring. Strong mitophagy activators could harm high-energy neurons if overdosed.
Timeline/cost: nutraceutical-style biomarker Phase 2: 2-4 years, $10-40M. Novel mitophagy drug: 5-8 years, $80-200M.
6. Retromer / Endosomal Trafficking
Feasibility: moderate; attractive but not trial-ready.
This is one of the cleaner mechanistic intersections between AD and PD, especially SORL1/VPS35 biology. It is less convincing for ALS/FTD except through broader endolysosomal stress.
Druggability: retromer stabilization is chemically plausible, but there is no mature clinical precedent. VPS35 gene therapy or overexpression is too early and safety-sensitive. Small-molecule chaperones or cargo-specific trafficking correctors are more realistic.
Best biomarkers: endosomal morphology in patient neurons, CI-MPR trafficking, APP processing/Aβ ratios, α-syn secretion/uptake, lysosomal enzyme trafficking, SORL1/VPS35 genotype, CSF Aβ/tau, α-syn SAA in PD.
Model systems: SORL1 loss-of-function iPSC neurons for AD; VPS35 D620N knock-in dopaminergic neurons for PD; microfluidic α-syn propagation assays. NHP α-syn PFF work is expensive and should wait until a molecule has strong rodent/human-cell data.
Clinical constraint: start with genetically enriched AD/PD subsets, not ALS/FTD. A pan-NDD indication would be unjustified.
Safety: vesicle trafficking is fundamental; chronic perturbation may affect synapses, lysosomal enzymes, immune cells, and peripheral organs.
Timeline/cost: discovery-to-IND: 3-5 years, $30-80M. First Phase 2 signal: 6-9 years, $120-250M.
7. Brain Insulin Resistance / Metabolic Dysregulation
Feasibility: low as a unifying therapeutic hypothesis; moderate as adjunctive stratification.
Druggability is easy: intranasal insulin, GLP-1 agonists, metformin-like AMPK modulation, IGF-1 axis drugs. The problem is specificity and endpoint clarity. ALS IGF-1 history is not encouraging, and AD/PD metabolic associations are heavily confounded by age, vascular disease, and systemic diabetes.
Best biomarkers: FDG-PET, insulin/IRS1 phospho-signaling in extracellular vesicles if analytically validated, HbA1c/insulin resistance, inflammatory-metabolic panels, cognition/motor endpoints by disease.
Clinical constraint: GLP-1 and metabolic drugs should be tested in metabolically enriched subgroups, not as generic AD/PD/ALS/FTD modifiers. ALS is especially risky because weight loss and hypermetabolism complicate metabolic intervention.
Safety: hypoglycemia for insulin approaches, weight loss/GI effects for GLP-1 agonists, frailty concerns in advanced NDD.
Timeline/cost: repurposed metabolic drug Phase 2: 2-4 years, $20-60M. New CNS metabolic drug: 5-8 years, $100M+.
Recommended Development Strategy
Prioritize three parallel tracks:
The investable thesis is not that all four diseases share one cause. It is that several stress-response systems recur across diseases, and the winning programs will use those systems to define treatable molecular subtypes.
Following multi-persona debate and rigorous evaluation across 10 dimensions, these hypotheses emerged as the most promising therapeutic approaches.
Interactive pathway showing key molecular relationships discovered in this analysis
graph TD
GBA1_mutations["GBA1 mutations"] -->|increases risk| PD["PD"]
TREM2_R47H_variant["TREM2 R47H variant"] -->|increases risk| Ad["Ad"]
alpha_synuclein_fibrils["alpha-synuclein fibrils"] -->|activates| NLRP3_Inflammasome["NLRP3 Inflammasome"]
TFEB_overexpression["TFEB overexpression"] -.->|inhibits| tau_A__pathology["tau/Aβ pathology"]
TARDBP_MUTATIONS["TARDBP MUTATIONS"] -->|causes| ALS_FTD["ALS/FTD"]
TDP_43_INCLUSIONS["TDP-43 INCLUSIONS"] -->|associated with| ALS_FTD_1["ALS/FTD"]
NfL_reduction["NfL reduction"] -->|biomarker for| als["als"]
TARDBP["TARDBP"] -->|cross disease mech| ALS["ALS"]
TARDBP_2["TARDBP"] -->|cross disease mech| FTD["FTD"]
TARDBP_3["TARDBP"] -->|cross disease mech| AD_LATE["AD/LATE"]
h_cross_synth_tdp43_rna_p["h-cross-synth-tdp43-rna-proteostasis"] -->|proposes shared me| TARDBP_4["TARDBP"]
SNCA["SNCA"] -->|cross disease mech| PD_5["PD"]
style GBA1_mutations fill:#ce93d8,stroke:#333,color:#000
style PD fill:#ef5350,stroke:#333,color:#000
style TREM2_R47H_variant fill:#ce93d8,stroke:#333,color:#000
style Ad fill:#ef5350,stroke:#333,color:#000
style alpha_synuclein_fibrils fill:#4fc3f7,stroke:#333,color:#000
style NLRP3_Inflammasome fill:#ce93d8,stroke:#333,color:#000
style TFEB_overexpression fill:#4fc3f7,stroke:#333,color:#000
style tau_A__pathology fill:#4fc3f7,stroke:#333,color:#000
style TARDBP_MUTATIONS fill:#ce93d8,stroke:#333,color:#000
style ALS_FTD fill:#ef5350,stroke:#333,color:#000
style TDP_43_INCLUSIONS fill:#4fc3f7,stroke:#333,color:#000
style ALS_FTD_1 fill:#ef5350,stroke:#333,color:#000
style NfL_reduction fill:#ce93d8,stroke:#333,color:#000
style als fill:#ef5350,stroke:#333,color:#000
style TARDBP fill:#4fc3f7,stroke:#333,color:#000
style ALS fill:#ef5350,stroke:#333,color:#000
style TARDBP_2 fill:#4fc3f7,stroke:#333,color:#000
style FTD fill:#ef5350,stroke:#333,color:#000
style TARDBP_3 fill:#4fc3f7,stroke:#333,color:#000
style AD_LATE fill:#ef5350,stroke:#333,color:#000
style h_cross_synth_tdp43_rna_p fill:#4fc3f7,stroke:#333,color:#000
style TARDBP_4 fill:#4fc3f7,stroke:#333,color:#000
style SNCA fill:#4fc3f7,stroke:#333,color:#000
style PD_5 fill:#ef5350,stroke:#333,color:#000
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Analysis ID: SDA-2026-04-28-cross-disease-synthesis
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