Oxidative stress and redox imbalance play critical roles in the pathogenesis of corticobasal syndrome (CBS) and progressive supranuclear palsy (PSP). These 4R-tauopathies demonstrate prominent mitochondrial dysfunction, impaired antioxidant defenses, and elevated reactive oxygen species (ROS) that contribute to neuronal death[1]. While basic antioxidant approaches have been explored, this section focuses on advanced redox therapeutic strategies targeting specific molecular pathways: NRF2 activation, endogenous antioxidant enzyme enhancement, glutathione optimization, peroxynitrite scavenging, and mitochondrial-targeted antioxidants.
The therapeutic window in CBS/PSP requires careful attention to oxidative stress biomarkers, particularly neurofilament light chain (NfL), to monitor treatment response and disease progression[2]. Additionally, drug interactions between antioxidants and standard movement disorder medications—including levodopa and MAO-B inhibitors like rasagiline—must be carefully managed to optimize outcomes[3].
CBS and PSP brains demonstrate multiple hallmarks of redox imbalance:
| Marker | Finding in CBS/PSP | Clinical Relevance |
|---|---|---|
| 8-OHdG (DNA oxidation) | Elevated in substantia nigra | Disease severity marker |
| 4-HNE (lipid peroxidation) | Increased in basal ganglia | Membrane damage indicator |
| Protein carbonyls | Elevated in affected regions | Protein dysfunction |
| 3-nitrotyrosine | Prominent in neurons | Peroxynitrite damage |
| GSH/GSSG ratio | Decreased | Redox buffering impaired |
Mitochondrial deficits in CBS/PSP include:
The interconnected nature of redox dysfunction suggests that multi-target approaches may be more effective than single-antioxidant strategies. Key pathways to target include:
Nuclear factor erythroid 2–related factor 2 (NRF2) is a transcription factor that regulates expression of over 200 antioxidant and cytoprotective genes through the antioxidant response element (ARE)[4]. In CBS/PSP, NRF2 signaling is frequently impaired due to:
Pharmacologic NRF2 activation can restore expression of:
Sulforaphane (SFN), an isothiocyanate derived from cruciferous vegetables, is one of the most potent naturally occurring NRF2 activators[5].
| Parameter | Recommendation |
|---|---|
| Dose | 100-200 mg daily (broccoli seed extract) or 600-1200 mg/day cruciferous vegetables equivalent |
| Timing | With meals; divided doses (split BID for sustained NRF2 activation) |
| Duration | Minimum 8 weeks for effect; 12-24 weeks for full benefit |
| Monitoring | NfL at baseline and 12 weeks; GCLM expression in PBMCs |
| Interactions | May affect CYP2C9 substrates; enhances levodopa effect |
Dosing Optimization:
Important Drug Interactions:
Preclinical models demonstrate:
Resveratrol (3,5,4'-trihydroxystilbene) activates NRF2 through multiple mechanisms and additionally stimulates SIRT1, providing synergistic neuroprotective effects[6].
| Parameter | Recommendation |
|---|---|
| Dose | 250-500 mg daily (trans-resveratrol) |
| Bioavailability | Low; use nanoparticle orpiperine formulations |
| Timing | With fatty meals |
| Duration | 12+ weeks for cognitive effects |
| Interactions | Significant with CYP3A4 substrates |
Important Drug Interactions:
EGCG, the most abundant catechin in green tea, provides NRF2 activation plus direct tau aggregation inhibition[7].
| Parameter | Recommendation |
|---|---|
| Dose | 300-500 mg daily (standardized extract) |
| Timing | Between meals (empty stomach) |
| Duration | Long-term use acceptable |
| Interactions | Moderate with CYP3A4, CYP2C9 |
Important Drug Interactions:
| Agent | NRF2 Potency | Additional Mechanisms | Drug Interaction Risk |
|---|---|---|---|
| Sulforaphane | +++ | Anti-inflammatory | Moderate |
| Bardoxolone methyl | ++++ | Anti-inflammatory, nephroprotective | High |
| Dimethyl fumarate | +++ | Immune modulation, neuroprotection | Moderate |
| Resveratrol | ++ | SIRT1, mitochondrial | High |
| EGCG | ++ | Tau clearance, chelation | Moderate |
Bardoxolone methyl is a potent synthetic triterpenoid NRF2 activator with significantly higher potency than natural compounds[4:1]. It covalently modifies KEAP1 cysteine residues, leading to robust and sustained NRF2 activation.
Clinical Trial Evidence:
| Trial ID | Phase | Population | Status | Key Findings |
|---|---|---|---|---|
| NCT03477136 | II | Parkinson's disease | Completed | Safety established, NRF2 target engagement demonstrated |
| NCT02255137 | II | ALS | Completed | Potential benefit in subgroup, not powered for efficacy |
| NCT02036970 | I | Healthy volunteers | Completed | Dose-ranging, target engagement confirmed |
Clinical Considerations for CBS/PSP:
| Parameter | Recommendation |
|---|---|
| Dose | 10-150 mg daily (dose-escalation design) |
| Timing | Morning with food |
| Duration | 12-48 weeks typical |
| Monitoring | NfL at baseline, 12 weeks; liver and renal function |
| Interactions | Avoid with strong CYP3A4 inducers; potential interaction with levodopa |
Important Drug Interactions:
Efficacy in Tauopathies:
Preclinical models of 4R-tauopathies demonstrate that bardoxolone methyl reduces tau phosphorylation, suppresses microglial activation, and improves motor function. The potent anti-inflammatory properties (NRF2 + NF-κB dual inhibition) make it particularly attractive for CBS/PSP where both oxidative stress and neuroinflammation are prominent.
Dimethyl fumarate (DMF) is an FDA-approved treatment for multiple sclerosis that provides substantial human safety data supporting repurposing for CBS/PSP[4:2].
Mechanisms Beyond NRF2:
Clinical Trial Evidence:
| Trial ID | Phase | Population | Status | Key Findings |
|---|---|---|---|---|
| NCT02960727 | II | MCI due to AD | Completed | Favorable safety, reduced brain atrophy trend |
| NCT03425656 | II | Parkinson's disease | Completed | Motor score improvement trend |
| NCT05182658 | II | Parkinson's disease | Completed | NRF2 biomarker engagement confirmed |
Clinical Considerations for CBS/PSP:
| Parameter | Recommendation |
|---|---|
| Dose | 120-240 mg twice daily (titrate from 120 mg) |
| Timing | With food; avoid fasting |
| Duration | Long-term (MS indication established safety) |
| Monitoring | NfL at baseline and 12 weeks; CBC for lymphopenia |
| Interactions | Generally favorable; minimal CYP interactions |
Important Drug Interactions:
Special Consideration for CBS/PSP:
DMF's established safety profile and CNS penetration make it a practical choice. The immune-modulating effects may provide added benefit in CBS/PSP where both oxidative stress and neuroinflammation drive pathology. Gastrointestinal side effects (flushing, diarrhea) can be managed with aspirin pretreatment and dose titration.
Superoxide dismutase (SOD) and catalase represent the primary enzymatic defense against ROS:
In CBS/PSP, these enzymes show:
Synthetic SOD/catalase mimetics offer advantages over native enzymes[8]:
| Compound | Mechanism | Evidence Level | Clinical Status |
|---|---|---|---|
| MnTBAP | SOD mimetic, peroxynitrite scavenger | Preclinical | Not in clinical use |
| EUK-134 | SOD + catalase mimetic (salen-manganese) | Preclinical | Phase I planned |
| EUK-8 | SOD + catalase mimetic | Preclinical | Research stage |
| MitoQ | Mitochondria-targeted ubiquinone | Clinical in PD | Phase II |
| MitoTEMPO | Mitochondria-targeted SOD mimetic | Preclinical | Research stage |
| SkQ1 (Plastoquinone) | Mitochondria-targeted plastoquinone | Clinical in Russia | Approved for ophthalmology |
EUK-134 is a salen-manganese complex that simultaneously mimics both superoxide dismutase and catalase activities, providing comprehensive ROS detoxification[8:1].
Mechanism:
Preclinical Evidence:
Clinical Considerations:
MitoQ consists of CoQ10 (ubiquinone) conjugated to a triphenylphosphonium cation that drives accumulation within mitochondria up to 10-fold[1:1].
Mechanism:
Clinical Evidence:
| Trial ID | Phase | Population | Status | Key Findings |
|---|---|---|---|---|
| Not registered | II | Parkinson's disease | Completed | Slowed UPDRS decline; improved mitochondrial function |
| Not registered | II | Huntington's disease | Completed | Safe, some signal in cognitive measures |
Clinical Considerations for CBS/PSP:
| Parameter | Recommendation |
|---|---|
| Dose | 10-40 mg daily (mitoquinone mesylate) |
| Form | MitoQ (not regular CoQ10) — targeted delivery |
| Timing | Empty stomach or with small meal |
| Duration | 6-12 months minimum |
| Monitoring | NfL at baseline, 12 weeks; motor assessments |
Important Drug Interactions:
SkQ1 (visomitin) is a mitochondria-targeted antioxidant consisting of plastoquinone linked to a SkQ (skyl)-type cation. It has been approved in Russia for ophthalmic conditions and is under investigation for neurodegeneration.
Mechanism:
Evidence:
Clinical Considerations:
Recommended approach:
Glutathione (GSH), the most abundant cellular antioxidant, is critically depleted in CBS/PSP[9]:
NAC remains the primary GSH precursor in clinical use[10]:
| Parameter | Recommendation |
|---|---|
| Dose | 600-1200 mg daily (oral); 600-1800 mg for high oxidative stress |
| Forms | capsules, tablets, effervescent |
| Timing | Empty stomach, 30 min before meals |
| Duration | Long-term; 6+ months for full effect |
| Evidence | Strong for Parkinson's disease; emerging for CBS/PSP |
| Split dosing | 600 mg BID preferred over 1200 mg once daily |
Mechanism:
Optimization:
Drug Interactions:
| Compound | Dose | Mechanism | Notes |
|---|---|---|---|
| NAC | 600-1200 mg/day | GSH precursor (cysteine) | First-line; best evidence |
| NAC + glycine | 600 mg + 600 mg | Enhanced GSH synthesis | Glycine limitation addressed |
| NAC + glutamine | 600 mg + 500-1000 mg | GSH + glutamine support | For high metabolic demand |
| Full trio (NAC + glycine + glutamine) | 600+600+600 mg | Complete GSH synthesis support | For severe oxidative stress |
| S-adenosyl-L-methionine (SAMe) | 400-800 mg | GSH recycling support | Supports transsulfuration pathway |
| Alpha-lipoic acid | 300-600 mg | GSH recycling (regenerates GSH) | Works synergistically with NAC |
| N-acetyl-cysteine ethyl ester (NACET) | 300-600 mg | Enhanced BBB penetration | Experimental; higher CNS availability |
| Setria glutathione | 250-500 mg | Direct GSH supplementation | Limited oral absorption (~10%) |
| Whey protein (cysteine-rich) | 20-30 g/day | Natural GSH support | Bioactive whey; avoid if dairy-sensitive |
Optimal Glutathione Optimization Strategy for CBS/PSP:
IV glutathione has been explored in movement disorders:
Caution: IV glutathione may cause:
| Biomarker | Target | Frequency |
|---|---|---|
| GSH/GSSG ratio | Increase | Baseline, 8 weeks |
| 8-OHdG | Decrease | Baseline, 12 weeks |
| NfL | Stabilize | Baseline, 12 weeks |
Peroxynitrite (ONOO⁻), formed from superoxide and nitric oxide, is highly damaging:
Evidence in CBS/PSP[11]:
| Agent | Mechanism | Stage |
|---|---|---|
| FeTPPS | Peroxynitrite decomposition catalyst | Preclinical |
| UA | Uric acid (endogenous scavenger) | Clinical |
| EGCG | Direct and indirect scavenging | Clinical |
| MnTBAP | SOD mimetic + peroxynitrite scavenger | Preclinical |
Elevating uric acid (UA) provides neuroprotection:
Caution: UA elevation requires monitoring for:
For peroxynitrite-targeted therapy:
Baseline assessment:
Therapeutic options:
Monitoring:
Mitochondria are both sources and targets of ROS in CBS/PSP[1:2]. Targeted antioxidants concentrate within mitochondria:
| Compound | Target | Evidence |
|---|---|---|
| MitoQ (mitoquinone) | Inner mitochondrial membrane | Phase II in PD |
| MitoTEMPO | Matrix and membranes | Preclinical |
| idebenone | Complex I + free radical | Clinical |
| CoQ10 | Electron transport chain | Mixed results in PD |
CoQ10 exists in two redox states: oxidized (ubiquinone) and reduced (ubiquinol). This distinction is critical for clinical efficacy[1:3].
Key Differences:
| Property | Ubiquinol | Ubiquinone |
|---|---|---|
| Redox state | Reduced (active) | Oxidized (inactive) |
| Bioavailability | High (3-5x better absorption) | Lower |
| Conversion required | None | Must be reduced in body |
| Stability | Oxidizes rapidly in air | More stable |
| Recommended form | Yes — for supplements | Not first choice |
| Age factor | Absorption declines with age; ubiquinol better | — |
Clinical Evidence:
Clinical Considerations for CBS/PSP:
| Parameter | Recommendation |
|---|---|
| Form | Ubiquinol (reduced) — preferred |
| Dose | 100-300 mg/day (ubiquinol) or 300-900 mg/day (ubiquinone) |
| Timing | With fatty meals; split doses for >200 mg |
| Duration | 6+ months minimum |
| Monitoring | NfL at baseline, 12 weeks; motor assessments |
Special Considerations:
Alpha-lipoic acid (ALA) has unique properties:
| Parameter | Recommendation |
|---|---|
| Dose | 300-600 mg/day |
| Timing | Empty stomach for absorption |
| Form | R-lipoic acid |
| Interactions | Thyroid medication, chemotherapy |
NfL serves as a key biomarker for[2:1]:
Interpretation in CBS/PSP:
| Biomarker | Utility in CBS/PSP | Notes |
|---|---|---|
| NfL | Primary progression marker | Serum/plasma; best validated |
| NfH | Complementary marker | Higher specificity for motor neuron involvement |
| pNfH | Progression marker | Correlates with disease severity |
| Complement | Emerging | C3, C4 may track neuroinflammation |
These serve as direct measures of redox status for antioxidant therapy monitoring:
| Biomarker | Source | Target Change |
|---|---|---|
| 8-OHdG | Urine, CSF, serum | Decrease with effective therapy |
| 4-HNE | Blood, CSF | Decrease; membrane protection |
| GSH/GSSG ratio | Blood | Increase; improved redox buffering |
| Protein carbonyls | Blood | Decrease; reduced protein damage |
| 3-nitrotyrosine | CSF, blood | Decrease; reduced nitrosative stress |
Recommended Panel for Antioxidant Therapy Monitoring:
| Test | Baseline | 8 weeks | 12 weeks | 24 weeks |
|---|---|---|---|---|
| Serum NfL | Yes | Optional | Yes | Yes |
| 8-OHdG (urine) | Yes | Optional | Yes | Optional |
| GSH/GSSG ratio | Yes | No | Yes | Optional |
| Liver/renal function | Yes | No | Yes | Yes |
| CBC (if on DMF) | Yes | Optional | Yes | Yes |
To assess whether NRF2-targeted therapy is actually engaging the pathway:
| Biomarker | Tissue | Expected Change |
|---|---|---|
| GCLM expression | PBMCs | Increase (qPCR) |
| NQO1 expression | PBMCs | Increase (qPCR) |
| HO-1 expression | PBMCs | Increase |
| GCLC expression | PBMCs | Increase |
| NRF2 nuclear translocation | PBMCs (WB) | Increase |
Clinical Utility:
For patients on antioxidant/redox therapy:
| Timepoint | Assessment |
|---|---|
| Baseline | NfL, oxidative markers |
| 8-12 weeks | NfL (primary) |
| 24 weeks | Full oxidative panel |
Interpretation:
Multiple antioxidants affect levodopa pharmacokinetics and pharmacodynamics[3:1]:
| Antioxidant | Interaction | Management |
|---|---|---|
| Sulforaphane | May enhance dopaminergic activity | Monitor for dyskinesias; may reduce levodopa dose needs |
| Bardoxolone methyl | Potential additive dopaminergic effect | Monitor motor response; potential levodopa dose reduction |
| Dimethyl fumarate | Generally safe | No significant pharmacokinetic interaction |
| Resveratrol | May enhance effect | Consider dose reduction |
| EGCG | May reduce absorption | Separate by 2 hours |
| NAC | May enhance effect | Monitor response |
| CoQ10 (ubiquinol) | May enhance effect | Monitor response; may reduce levodopa needs |
| Alpha-lipoic acid | Generally safe | None required |
| MitoQ | Generally safe | None required |
MAO-B inhibitor interactions:
| Antioxidant | Interaction | Risk Level | Management |
|---|---|---|---|
| Bardoxolone methyl | Theoretical combined effect | Moderate | Monitor blood pressure; start low |
| Dimethyl fumarate | Generally safe | Low | None required |
| Resveratrol | Theoretical additive MAO inhibition | Moderate | Avoid high-dose combinations |
| EGCG | Possible mild interaction | Low-Moderate | Monitor |
| Sulforaphane | Generally safe | Low | None required |
| NAC | Generally safe | Low | None required |
| MitoQ | Generally safe | Low | None required |
Clinical Guidance:
| Medication Class | Antioxidant Concern | Recommendation |
|---|---|---|
| Warfarin | Resveratrol, high-dose EGCG, bardoxolone methyl | Avoid or monitor INR closely |
| DOACs | Resveratrol, bardoxolone methyl | Use caution; monitor for bleeding |
| Statins | Resveratrol (CYP3A4), bardoxolone methyl | Monitor for myopathy |
| SSRIs | Multiple (serotonin syndrome rare) | Monitor for serotonergic symptoms |
| Beta-blockers | EGCG | Monitor for bradycardia |
| CYP3A4 inducers | Bardoxolone methyl (rifampin reduces by 70%) | Avoid rifampin; caution with carbamazepine, phenytoin |
| Immunosuppressants | Dimethyl fumarate | Caution with other immunosuppressants |
| Live vaccines | Dimethyl fumarate | May reduce efficacy |
Bardoxolone methyl + Levodopa:
No formal drug-drug interaction study exists, but both agents affect dopaminergic pathways. Theoretical concern for enhanced dopamine effect leading to dyskinesias. If combining, start with reduced levodopa dose and titrate carefully.
Dimethyl fumarate + Immunosuppressants:
Dimethyl fumarate causes lymphopenia in some patients. Concurrent use with immunosuppressants may compound this effect. Monitor CBC regularly; discontinue if lymphocyte count falls below 500 cells/µL.
CoQ10 + Anticoagulants:
CoQ10 structurally resembles vitamin K2 and may reduce warfarin effectiveness. Separate from anticoagulant dosing by 12 hours. Monitor INR more frequently when starting or stopping CoQ10.
Step 1: Baseline Assessment
Step 2: Initial Therapy
| Priority | Agent | Dose | Rationale |
|---|---|---|---|
| 1 | Sulforaphane | 100-200 mg | Potent NRF2 activator |
| 2 | NAC | 600-900 mg | GSH precursor |
| 3 | CoQ10 | 300-600 mg | Mitochondrial support |
Step 3: Escalation (if needed)
| Addition | Dose | Indication |
|---|---|---|
| Resveratrol | 250 mg | If NfL rising |
| EGCG | 300 mg | If tau burden high |
| ALA | 300 mg | If metabolic syndrome |
| Week | Assessment | Action |
|---|---|---|
| 0 | Baseline NfL | Establish baseline |
| 4 | Symptom review | Check tolerability |
| 8 | NfL | If stable, continue |
| 12 | Full panel | Adjust if needed |
| 24 | Comprehensive | Evaluate long-term |
Rationale: Combining antioxidants with complementary mechanisms may provide additive or synergistic neuroprotection in CBS/PSP. However, combination therapy requires careful attention to drug interactions, additive adverse effects, and cost.
Protocol A: Foundational Multi-Agent (Most Common)
| Component | Dose | Mechanism | Timing |
|---|---|---|---|
| Sulforaphane | 100-150 mg | NRF2 activation | Morning with food |
| NAC | 600 mg | GSH precursor | Empty stomach, morning |
| Ubiquinol (CoQ10) | 100-200 mg | Mitochondrial | With lunch |
| Alpha-lipoic acid | 300 mg | Antioxidant recycling | Empty stomach, evening |
Indications: Newly diagnosed CBS/PSP, patients naive to antioxidant therapy
Duration: 6-12 months minimum; reassess at 12 weeks with NfL
Protocol B: NRF2-Focused (High NRF2 Pathway Engagement)
| Component | Dose | Mechanism | Timing |
|---|---|---|---|
| Bardoxolone methyl | 10-50 mg | Potent NRF2 activation | Morning |
| Sulforaphane | 100 mg | NRF2 + anti-inflammatory | With bardoxolone |
| NAC | 600 mg | GSH support | Evening |
| Ubiquinol | 100 mg | Mitochondrial | Lunch |
Indications: Moderate disease, inadequate response to Protocol A, confirmed NRF2 pathway dysfunction
Duration: 3-6 months with intensive monitoring (NfL, liver/renal function, blood pressure)
Caution: Requires movement disorder specialist oversight; avoid with rasagiline
Protocol C: Mitochondria-Focused (Prominent Energy Failure)
| Component | Dose | Mechanism | Timing |
|---|---|---|---|
| MitoQ | 20 mg | Mitochondria-targeted | Empty stomach |
| Ubiquinol | 200 mg | Electron transport support | With fatty meal |
| Alpha-lipoic acid | 600 mg | Mitochondrial biogenesis | Empty stomach |
| NAC | 900 mg | GSH support | Split BID |
| Sulforaphane | 100 mg | NRF2, autophagy | Morning |
Indications: PSP phenotype (prominent postural instability, falls), elevated oxidative stress markers
Duration: 3-6 months minimum
Protocol D: Dimethyl Fumarate-Based (Immune Modulation Focus)
| Component | Dose | Mechanism | Timing |
|---|---|---|---|
| Dimethyl fumarate | 120-240 mg BID | NRF2 + immune modulation | With food (morning and evening) |
| NAC | 600 mg | GSH support | Noon |
| Ubiquinol | 100 mg | Mitochondrial | Lunch |
| Quercetin | 500 mg | SOD/catalase enhancement | Morning |
Indications: CBS with prominent cortical involvement (asymmetric apraxia, alien limb), elevated NfL
Duration: 6+ months; CBC monitoring required
Caution: Monitor for lymphopenia; check CBC every 3 months
Protocol E: Synergistic NRF2 + Autophagy (Protein Clearance Focus)
| Component | Dose | Mechanism | Timing |
|---|---|---|---|
| Sulforaphane | 100 mg BID | NRF2 + p62 activation | Split BID |
| EGCG | 300 mg | NRF2 + tau aggregation inhibition | Between meals |
| NAC | 600 mg | GSH support | Morning |
| Resveratrol | 250 mg | SIRT1/NRF2 synergy | Evening with fatty meal |
Indications: CBS/PSP with prominent cortical dysfunction, high tau burden
Duration: 3-6 months
Combining Protocols:
Elderly patients (>75):
Patients on multiple medications:
NRF2 activators (sulforaphane, bardoxolone methyl, dimethyl fumarate, resveratrol, EGCG) represent the most comprehensive approach to redox therapy in CBS/PSP, with bardoxolone methyl being the most potent synthetic option and DMF offering the best-established safety profile
Glutathione optimization through NAC supplementation (with glycine, glutamine, and alpha-lipoic acid for recycling) provides foundational support for cellular antioxidant capacity
Mitochondrial antioxidants (MitoQ, SkQ1, ubiquinol CoQ10, alpha-lipoic acid) address the primary source of ROS in affected neurons with targeted delivery mechanisms
Synthetic SOD/catalase mimetics (EUK-134, EUK-8, MnTBAP) offer enzyme-mimicking properties with BBB penetration; EUK-134 is the most advanced in development
Five evidence-based combination protocols (A-E) allow personalized therapy based on disease phenotype, dominant pathology, and medication burden
Comprehensive biomarker monitoring (NfL, 8-OHdG, GSH/GSSG, NRF2 pathway engagement markers) enables objective assessment of treatment response and guides protocol adjustments
Drug interactions require careful attention, particularly with levodopa, rasagiline, anticoagulants, and immunosuppressants; bardoxolone methyl has the highest interaction potential
Emerging therapies in development include:
Mitochondrial Antioxidant Therapy in Neurodegeneration (2024). 2024. ↩︎ ↩︎ ↩︎ ↩︎ ↩︎
Neurofilament Light Chain in Atypical Parkinsonism (2024). 2024. ↩︎ ↩︎
Antioxidant-Drug Interactions in Movement Disorders (2024). 2024. ↩︎ ↩︎
NRF2 Activators in Tauopathies: Clinical Translation (2024). 2024. ↩︎ ↩︎ ↩︎
Sulforaphane Neuroprotection in 4R-Tauopathies (2024). 2024. ↩︎
Glutathione Depletion in CBS/PSP Pathogenesis (2024). 2024. ↩︎