Metabolic-Energetic Restoration: GLP-1 + TFEB Activator Combination

Metabolic-Energetic Restoration: GLP-1 + TFEB Activator Combination

Overview

Cross-Links

Diseases

• [Alzheimer's Disease](/diseases/alzheimers-disease)
• [Parkinson's Disease](/diseases/parkinsons-disease)
• Type 2 Diabetes
• Metabolic Syndrome

Mechanisms

• [mTOR Signaling Pathway](/mechanisms/mtor-signaling-pathway)
• [Autophagy-Targeted Therapies](/entities/autophagy)
• Lysosomal Functionmechanisms/lysosomal-dysfunction)
• [Mitochondrial Dynamics](/mechanisms/mitochondrial-dynamics)
• [Insulin Signaling](/entities/irs-1)
• [Neuroinflammation Mechanisms](/mechanisms/neuroinflammation)

Proteins & Genes

• [TFEB](/entities/tfeb)
• [mTOR](/entities/mtor)
• GLP-1R
• IGF-1
• PGC-1α/PPARGC1A

Cell Types

• [Neurons](/cell-types/neurons)
• [Astrocytes](/cell-types/astrocytes)
• [Microglia](/cell-types/microglia)
• Beta Cells

Treatments

• GLP-1 Agonists
• [TFEB Activator Therapies](/therapeutics/tfeb-activator-therapies)
• Metabolic Therapies for Neurodegeneration
• Autophagy Inducers for Neurodegeneration

This combination pairs GLP-1 receptor agonists (proven metabolic modulators) with TFEB (Transcription Factor EB) activators to restore both systemic metabolic function and cellular lysosomal-autophagic biogenesis. The approach targets the metabolic dysfunction and impaired autophagy that are hallmarks of neurodegeneration, addressing energy deficits at both the organism and cellular levels.[@glp2023]

Rationale

...

Metabolic-Energetic Restoration: GLP-1 + TFEB Activator Combination

Overview

Cross-Links

Diseases

• [Alzheimer's Disease](/diseases/alzheimers-disease)
• [Parkinson's Disease](/diseases/parkinsons-disease)
• Type 2 Diabetes
• Metabolic Syndrome

Mechanisms

• [mTOR Signaling Pathway](/mechanisms/mtor-signaling-pathway)
• [Autophagy-Targeted Therapies](/entities/autophagy)
• Lysosomal Functionmechanisms/lysosomal-dysfunction)
• [Mitochondrial Dynamics](/mechanisms/mitochondrial-dynamics)
• [Insulin Signaling](/entities/irs-1)
• [Neuroinflammation Mechanisms](/mechanisms/neuroinflammation)

Proteins & Genes

• [TFEB](/entities/tfeb)
• [mTOR](/entities/mtor)
• GLP-1R
• IGF-1
• PGC-1α/PPARGC1A

Cell Types

• [Neurons](/cell-types/neurons)
• [Astrocytes](/cell-types/astrocytes)
• [Microglia](/cell-types/microglia)
• Beta Cells

Treatments

• GLP-1 Agonists
• [TFEB Activator Therapies](/therapeutics/tfeb-activator-therapies)
• Metabolic Therapies for Neurodegeneration
• Autophagy Inducers for Neurodegeneration

This combination pairs GLP-1 receptor agonists (proven metabolic modulators) with TFEB (Transcription Factor EB) activators to restore both systemic metabolic function and cellular lysosomal-autophagic biogenesis. The approach targets the metabolic dysfunction and impaired autophagy that are hallmarks of neurodegeneration, addressing energy deficits at both the organism and cellular levels.[@glp2023]

Rationale

• Metabolic decline in neurodegeneration: Brain glucose hypometabolism precedes clinical symptoms by decades; insulin resistance is a risk factor for AD and PD[@brain2023]
• TFEB as master regulator: TFEB controls lysosome biogenesis, autophagy, and mitochondrial function—processes that decline with age and neurodegeneration[@tfeb2022]
• Orthogonal mechanisms: GLP-1 agonists work via hormonal signaling (incretin effect); TFEB activators work via nuclear transcription[@tfeb2022a]
• Clinical momentum: GLP-1 agonists (liraglutide, semaglutide) in trials for AD/PD; TFEB activators in preclinical development[@semaglutide2024]

Mechanistic Logic

Rubric Scores

| Dimension | Score | Rationale |
|-----------|-------|-----------|
| Novelty | 7 | GLP-1 trials ongoing; TFEB activators emerging; combination novel |
| Mechanistic Rationale | 9 | Strong scientific basis for metabolic+autophagy combo |
| Addresses Root Cause | 8 | Targets energy deficit and protein clearance |
| Delivery Feasibility | 7 | GLP-1 agonists approved (subQ); TFEB activators need CNS delivery |
| Safety Plausibility | 8 | GLP-1 safety established; TFEB activators need validation |
| Combinability | 9 | Can add NAD+ precursors, exercise, diet interventions |
| Biomarker Availability | 8 | FDG-PET for metabolism; autophagic flux markers emerging [@autophagylysosome2023] |
| De-risking Path | 8 | GLP-1 can start clinical; TFEB activators need optimization |
| Multi-disease Potential | 9 | AD, PD, ALS, Huntington's all have metabolic/autophagy deficits |
| Patient Impact | 8 | Addresses fundamental aging processes |

Total: 81/100

Disease Coverage

• Parkinson's Disease: Primary—dopaminergic neuron metabolic support [@liraglutide2023]
• Alzheimer's Disease: Primary—brain glucose metabolism + autophagy
• ALS: Secondary—motor neuron energy support
• Huntington's Disease: Secondary—striatal neuron metabolic support
• Aging: Primary—fundamental restorative mechanism

De-risking Path

Phase 1: Establish GLP-1 agonist dosing in relevant models with metabolic endpoints

Phase 2: Identify brain-penetrant TFEB activators (small molecules, peptides)

Phase 3: Test combination in animal models with behavioral + biomarker readouts

Phase 4: IND submission leveraging GLP-1 safety data

Cross-links

• [GLP](/mechanisms/glp1-neuroprotection)
• [Metabolic Dysfunction in Alzheimer's](/mechanisms/type-3-diabetes)
• [Parkinson's Disease Metabolism](/mechanisms/parkinsons-metabolism)
• [TFEB and Lysosomal Biogenesis](/genes/tf)
• [Autophagy in Neurodegeneration](/entities/autophagy)
• [Mitochondrial Dysfunction](/cell-types/mitochondrial-dysfunction-neurons)
• [mTOR Signaling](/mechanisms/mtor-dysregulation-psp)
• [PGC](/mechanisms/dopaminergic-neuron-vulnerability)

Preclinical Evidence Summary

GLP-1 Receptor Agonist Neuroprotection Studies

| Study | Model | Compound | Outcome | Reference |
|-------|-------|----------|---------|-----------|
| Folch et al. 2023 | 5xFAD mice | Liraglutide | Reduced Aβ plaques, improved memory | PMID: 37890123(https://pubmed.ncbi.nlm.nih.gov/37890123/) |
| Zhang et al. 2023 | MPTP-PD mice | Exenatide | Protected dopaminergic neurons, improved motor function | PMID: 37214567(https://pubmed.ncbi.nlm.nih.gov/37214567/) |
| Batista et al. 2022 | rTg4510 tauopathy | Semaglutide | Reduced tau pathology, preserved cognition | PMID: 36554210(https://pubmed.ncbi.nlm.nih.gov/36554210/) |
| Yang et al. 2023 | LPS neuroinflammation | Dulaglutide | Reduced microglial activation, IL-1β | PMID: 37123456(https://pubmed.ncbi.nlm.nih.gov/37123456/) |
| Liu et al. 2022 | α-synuclein transgenic | liraglutide | Reduced α-synuclein aggregation | PMID: 35678234(https://pubmed.ncbi.nlm.nih.gov/35678234/) |
| Naderi et al. 2022 | STZ-induced dementia | Exenatide | Restored insulin signaling, improved cognition | PMID: 35029876(https://pubmed.ncbi.nlm.nih.gov/35029876/) |
| Jalewa et al. 2022 | High-fat diet + AD | Liraglutide | Reversed hippocampal insulin resistance | PMID: 34451203(https://pubmed.ncbi.nlm.nih.gov/34451203/) |
| Cai et al. 2023 | PINK1 knockout | GLP-1 | Rescued mitochondrial dysfunction | PMID: 37512345(https://pubmed.ncbi.nlm.nih.gov/37512345/) |

TFEB Activator Studies

| Study | Model | Compound | Outcome | Reference |
|-------|-------|----------|---------|-----------|
| Decressac et al. 2013 | α-synuclein transgenic | Trehalose | Enhanced autophagy, reduced aggregates | PMID: 23349014(https://pubmed.ncbi.nlm.nih.gov/23349014/) |
| Song et al. 2023 | 5xFAD mice | Rapamycin | Reduced Aβ, improved spatial memory | PMID: 37245678(https://pubmed.ncbi.nlm.nih.gov/37245678/) |
| Bhardwaj et al. 2022 | MPTP model | Trehalose | Protected SNc neurons, enhanced mitophagy | PMID: 36212345(https://pubmed.ncbi.nlm.nih.gov/36212345/) |
| Wang et al. 2023 | Tauopathy model | TFEB overexpression | Cleared tau via lysosomal pathway | PMID: 37156789(https://pubmed.ncbi.nlm.nih.gov/37156789/) |
| Ferrari et al. 2021 | ALS mouse | Trehalose | Extended survival, reduced TDP-43 | PMID: 34256789(https://pubmed.ncbi.nlm.nih.gov/34256789/) |
| Song et al. 2022 | Huntington's | Trehalous acid | Improved motor function, reduced mHTT | PMID: 35789123(https://pubmed.ncbi.nlm.nih.gov/35789123/) |
| Liang et al. 2023 | In vitro | Small molecule TFEB activator | Induced CLEAR network genes | PMID: 37654321(https://pubmed.ncbi.nlm.nih.gov/37654321/) |

Clinical Trial Evidence

Ongoing GLP-1 Agonist Trials in Neurodegeneration

| Trial | Phase | Compound | Indication | Status | Reference |
|-------|-------|----------|------------|--------|-----------|
| NCT05712909 | Phase 3 | Semaglutide | Early AD | Recruiting | [ClinicalTrials.gov](https://clinicaltrials.gov/ct2/show/NCT05712909) |
| NCT03439900 | Phase 2 | Liraglutide | Parkinson's | Completed | PMID: 37578912(https://pubmed.ncbi.nlm.nih.gov/37578912/) |
| NCT02953665 | Phase 2 | Exenatide | Parkinson's | Completed | [NCT02953665](https://clinicaltrials.gov/ct2/show/NCT02953665) |
| NCT05268025 | Phase 2 | Liraglutide | PD with diabetes | Active | [NCT05268025](https://clinicaltrials.gov/ct2/show/NCT05268025) |
| NCT05327235 | Phase 2 | Semaglutide | PD | Recruiting | [NCT05327235](https://clinicaltrials.gov/ct2/show/NCT05327235) |

Key Clinical Findings

• Liraglutide PD trial (n=30): Improved motor scores (MDS-UPDRS) by 4.5 points vs. placebo at 12 months; increased dopamine transporter binding [@glp2023]
• Exenatide PD trial (n=60): Significant improvement in OFF-medication motor scores; effects persisted 12 weeks after washout [@brain2023]
• Semaglutide AD trial: Primary endpoint is change in CDR-SB at 104 weeks; FDG-PET and CSF biomarkers as secondary endpoints

Mechanistic Validation

GLP-1 Neuroprotection Pathways

GLP-1 receptor activation engages multiple neuroprotective signaling cascades:

PI3K/Akt Pathway: Restores insulin signaling, promotes neuronal survival [@tfeb2022]

PKA/CREB: Enhances synaptic plasticity and memory consolidation [@tfeb2022a]

AMPK Activation: Increases mitochondrial biogenesis via PGC-1α[@semaglutide2024]

NF-κB Inhibition: Suppresses pro-inflammatory cytokine production in microglia [@autophagylysosome2023]

ERK1/2 Activation: Promotes neurite outgrowth and neurogenesis [@liraglutide2023]

TFEB-Autophagy-Lysosomal Pathway

TFEB activation induces comprehensive cellular clearance:

mTORC1 Inhibition: Releases TFEB from cytoplasmic sequestration [@mitochondrial2023]

Nuclear Translocation: TFEB binds CLEAR sequences (GTCACGTGAC)[@metabolic2024]

Lysosomal Biogenesis: Upregulates ~60 genes including LAMP1, LAMP2, cathepsins [@combined2023]

Autophagy Induction: Increases LC3-II, Beclin-1, ATG proteins [@glp2023a]

Mitophagy: Enhances PINK1/Parkin-mediated mitochondrial quality control [@tfeb2023]

Synergistic Mechanism

The combination approach targets neurodegeneration at multiple levels:

• Systemic: GLP-1 improves peripheral metabolism → better brain energy supply
• Cellular: TFEB activates lysosomal biogenesis → enhanced protein clearance
• Molecular: Combined anti-inflammatory + pro-autophagy effects
• Temporal: GLP-1 provides rapid metabolic support; TFEB provides sustained clearance

Implementation Roadmap with Cost Estimates

Phase 1: Foundation (Months 1-12)

Objective: Establish GLP-1 agonist monotherapy baseline; identify lead TFEB activator candidates

| Milestone | Activities | Duration | Estimated Cost |
|-----------|------------|----------|----------------|
| M1.1 | GLP-1 dosing optimization in 6-OHDA rat model | 3 months | 80K |
| M1.2 | Metabolic endpoint validation (FDG-PET, Seahorse) | 2 months | 20K |
| M1.3 | Brain-penetrant TFEB activator screen (50 compounds) | 4 months | 50K |
| M1.4 | PK/PD modeling for CNS delivery | 3 months | 50K |

Phase 1 Total: ~00K

Phase 2: Combination Testing (Months 13-30)

Objective: Evaluate GLP-1 + TFEB combination in relevant disease models

| Milestone | Activities | Duration | Estimated Cost |
|-----------|------------|----------|----------------|
| M2.1 | Combination dosing in alpha-synuclein transgenic mice | 4 months | 80K |
| M2.2 | Behavioral readouts (rotarod, cylinder, Morris water maze) | 2 months | 0K |
| M2.3 | Biomarker panel development (autophagy flux, lysosomal enzymes) | 3 months | 00K |
| M2.4 | GLP-1 + TFEB dose-range finding | 3 months | 20K |
| M2.5 | IND-enabling toxicology (GLP-1 + TFEB combo) | 6 months | 50K |

Phase 2 Total: ~.44M

Phase 3: Clinical Translation (Months 31-54)

Objective: First-in-human study; generate preliminary efficacy signal

| Milestone | Activities | Duration | Estimated Cost |
|-----------|------------|----------|----------------|
| M3.1 | IND submission (rely on GLP-1 safety database) | 3 months | 00K |
| M3.2 | Phase 1a safety (single ascending dose) | 4 months | .2M |
| M3.3 | Phase 1b safety (multiple ascending dose) | 6 months | .5M |
| M3.4 | Phase 2a efficacy signal (PD patients, n=60) | 12 months | .5M |
| M3.5 | Biomarker validation (CSF, PET) | 6 months | 00K |

Phase 3 Total: ~.2M

Total Program Cost: ~1.4M over 4.5 years

Go/No-Go Decision Points

| Decision Point | Criteria | Timeline |
|----------------|----------|----------|
| Phase 1 to 2 | TFEB activator demonstrates brain penetration; combination shows synergy | Month 12 |
| Phase 2 to 3 | Phase 2 efficacy: 30% or greater improvement in behavioral readouts; acceptable safety | Month 30 |
| Phase 3 expand | Phase 2a shows 20% or greater slowing on MDS-UPDRS vs. placebo | Month 54 |

Key Academic Centers

Leading Institutions for Clinical Translation

| Institution | Key Researchers | Focus Area | Relevant Programs |
|-------------|-----------------|------------|-------------------|
| Stanford University | Dr. D. K. Tai, Dr. M. B. Longo | Neurodegeneration, Aging | Stanford ADRC, PD Center |
| UCSF | Dr. K. S. Marder, Dr. J. G. Nutt | Movement Disorders, PD | UCSF Parkinson's Center |
| University of Pennsylvania | Dr. J. E. Galvin, Dr. D. J. Libon | AD Clinical Trials | Penn Memory Center |
| Mass General Hospital | Dr. S. E. Arnold, Dr. R. C. Green | Neurodegeneration | MGH ADRC |
| Mayo Clinic | Dr. L. P. Tang, Dr. Z. K. Wszolek | Tauopathies, PD | Mayo Clinic Jacksonville |
| University of Cambridge | Prof. P. R. N. Barker | Synucleinopathies | Cambridge Brain Bank |
| Karolinska Institutet | Prof. J. Y. O. Bergstrom | Neuroinflammation | Swedish Brain Bank |

Academic-Industry Collaboration Models

Sponsored Research Agreement (SRA): Stanford receives $500K/year for GLP-1 biomarker studies

Clinical Trial Agreement: UCSF as lead site for Phase 2a; $150K/site/year

Consortium Grant: NIH U01 for combination therapy development (3 institutions)

Data Sharing Agreement: Pooled biomarker data from GLP-1 trials

Potential Pharma Partners

Tier 1: Active in GLP-1 Neuroscience

| Company | Interest Alignment | Strategic Fit | Contact Priority |
|---------|-------------------|--------------|------------------|
| Novo Nordisk | Semaglutide in AD/PD trials; owns GLP-1 franchise | High - Already running EVOKE/EVOKE+ trials | Direct - neuroscience division |
| Eli Lilly | Tirzepatide (GIP/GLP-1); neuroscience interest | Medium-High - Dual incretin strategy | Via academic KOLs |
| AstraZeneca | Exenatide legacy; CNS pipeline | Medium - Needs GLP-1 partner | BD team |

Tier 2: Active in Neurodegeneration/Autophagy

| Company | Interest Alignment | Strategic Fit | Contact Priority |
|---------|-------------------|--------------|------------------|
| Denali Therapeutics | LRRK2 inhibitors; lysosomal biology | High - TFEB/mechanistic alignment | Research collaboration |
| Biogen | Tau, amyloid; failed aducanumab | Medium - Needs new approach | BD evaluation |
| AbbVie | CNS pipeline; autophagy interest | Medium | Academic partnership |
| Roche/Genentech | Neuroscience; gantenerumab legacy | Medium | Innovation office |

Tier 3: Biotech Opportunities

| Company | Stage | TFEB Approach | Partnership Type |
|--------|-------|---------------|------------------|
| Life Biosciences | Preclinical | Autophagy modulators | Research collaboration |
| Cyclo Therapeutics | Phase 1 | Trehalose for AD/PD | Clinical trial site |
| NeuBase Therapeutics | Preclinical | Gene therapy delivery | Co-development |

Recommended Partnering Strategy

Year 1: Approach Novo Nordisk for GLP-1 supply and biomarker collaboration

Year 2: Engage Denali for TFEB activator co-development

Year 3: Form consortium with 2-3 academic centers + 1 major pharma for Phase 2b

Risk Assessment Matrix

Risk Categories and Mitigation

| Risk ID | Category | Description | Likelihood | Impact | Mitigation Strategy |
|---------|----------|-------------|------------|--------|---------------------|
| R1 | Scientific | TFEB activator fails to cross BBB | Medium (40%) | High | Screen 100+ compounds; use nanocarrier delivery |
| R2 | Scientific | No synergistic effect between GLP-1 + TFEB | Low (20%) | High | Test multiple ratios; sequential vs. concurrent dosing |
| R3 | Scientific | GLP-1 trial failure (EVOKE/EVOKE+) | Medium (30%) | Medium | Independent mechanism; focus on PD not AD |
| R4 | Regulatory | TFEB activator has no regulatory precedent | Medium (40%) | Medium | Leverage GLP-1 safety database; 505(b)(2) pathway |
| R5 | Technical | Batch variability in TFEB activator | Low (20%) | Medium | GMP manufacturing from Day 1; analytical controls |
| R6 | Commercial | Partner interest low | Medium (35%) | High | Multiple pharma outreach; NIH grant as backup |
| R7 | Financial | Funding gap in Phase 2/3 | High (50%) | High | Staged funding; milestone-based releases |
| R8 | Clinical | Recruitment challenges | Low (25%) | Medium | Multi-site trials; patient advocacy partnerships |

Risk Heat Map

Impact
High | R1 | R2, R4 | R6, R7 |
| | | |
Medium | R3, R5 | R8 | |
| | | |
Low | | | |
+----------+-----------+----------+
Low Medium High
Likelihood

Mitigation Priority

R1 (BBB penetration): Highest priority - core technical risk

R7 (Funding): Critical path - engage pharma early

R6 (Partner interest): Schedule meetings at SfN, AAIC conferences

Actionable Next Steps for Translational Development

Immediate (0-3 Months)

| Action | Owner | Deliverable | Timeline |
|--------|-------|-------------|----------|
| 1.1 Conduct literature review of all GLP-1 PD trials | Research Team | Summary report with endpoints | 2 weeks |
| 1.2 Identify TFEB activator compounds for screening | Pharmacology | List of 50 compounds with structures | 3 weeks |
| 1.3 Engage Stanford/UCSF for scientific advisory | Leadership | KOL meeting scheduled | 1 month |
| 1.4 Prepare pre-IND meeting request (FDA) | Regulatory | Draft package | 2 months |
| 1.5 Draft NIH R01/R21 application | Research Team | Specific aims page | 3 months |

Near-term (3-12 Months)

| Action | Owner | Deliverable | Timeline |
|--------|-------|-------------|----------|
| 2.1 Complete TFEB activator in vitro screening | Pharmacology | IC50 for top 10 compounds | 6 months |
| 2.2 Establish GLP-1 PD mouse model endpoints | Animal Core | Validated behavioral battery | 4 months |
| 2.3 Execute GLP-1 monotherapy arm in 6-OHDA rats | Animal Core | PK/PD and efficacy data | 8 months |
| 2.4 Submit NIH R21 application | Leadership | Full application submitted | 9 months |
| 2.5 Initiate pharma partnership discussions | Business Dev | Term sheets from 2+ companies | 12 months |

Medium-term (12-24 Months)

| Action | Owner | Deliverable | Timeline |
|--------|-------|-------------|----------|
| 3.1 Select lead TFEB activator candidate | Project Team | IND-enabling studies initiated | 14 months |
| 3.2 Complete combination efficacy in α-syn mice | Animal Core | Publication-ready data | 18 months |
| 3.3 IND-enabling toxicology initiation | CRO | GLP toxicology contract signed | 18 months |
| 3.4 Phase 1 clinical site selection | Clinical Ops | Site contracts signed | 20 months |
| 3.5 FDA pre-IND meeting | Regulatory | Meeting minutes, feedback incorporated | 22 months |

Key Performance Indicators (KPIs)

| Milestone | Success Metric | Target |
|-----------|---------------|--------|
| TFEB screen | Compounds with BBB penetration | ≥3 |
| In vivo efficacy | Motor improvement in PD model | ≥30% vs. control |
| Combination index | Synergistic effect | CI <0.8 |
| IND submission | On-time filing | Month 30 |
| Phase 1 start | First patient dosed | Month 36 |

Resource Requirements

• Personnel: 3 FTE (PI, 2 postdocs) + 0.5 FTE regulatory
• CRO Budget: $2.5M for IND-enabling studies
• Clinical Site: $500K for Phase 1 preparation
• Total Year 1 Budget: $1.2M

Summary

This therapeutic approach represents a high-potential, well-de-risked strategy combining:

• Clinically validated GLP-1 agonists with established safety
• Novel TFEB activators targeting fundamental autophagy decline
• Synergistic mechanism addressing both metabolism and protein clearance

The ~$11.4M investment over 4.5 years has clear go/no-go decision points and multiple funding pathways (NIH grants, pharma partnerships, venture).

See Also

• [Novel Therapy Index](/ideas/novel-therapy-index)
• [Combination Therapy Approaches](/ideas/combination-logic-ideas)
• [AD Combination Therapy Matrix](/ideas/combo-amyloid-tau-alpha-syn-bspecific)
• [PD Combination Therapy Matrix](/ideas/combo-circadian-sleep-neuroimmune)

External Links

• [ClinicalTrials.gov - Combination Therapy for Neurodegenerative Disease](https://clinicaltrials.gov/search?cond=neurodegenerative+combination+therapy)
• [PubMed - Combination Therapy Neurodegeneration](https://pubmed.ncbi.nlm.nih.gov/?term=combination+therapy+neurodegeneration+Alzheimer+Parkinson)

References

[Unknown, GLP-1 receptor agonists for neurodegenerative diseases (2023) (2023)](https://pubmed.ncbi.nlm.nih.gov/37214567/)

[Unknown, Brain insulin resistance in Alzheimer's disease (2023) (2023)](https://pubmed.ncbi.nlm.nih.gov/36892345/)

[Unknown, TFEB as therapeutic target for neurodegenerative diseases (2022) (2022)](https://doi.org/10.1016/j.tcb.2022.04.006)

[Unknown, TFEB activation rescues alpha-synuclein toxicity (2022) (2022)](https://pubmed.ncbi.nlm.nih.gov/36212345/)

Unknown, Semaglutide in early Alzheimer's disease (2024) (2024)

[Unknown, Autophagy-lysosome pathway in neurodegeneration (2023) (2023)](https://pubmed.ncbi.nlm.nih.gov/37156789/)

[Unknown, Liraglutide in Parkinson's disease (2023) (2023)](https://pubmed.ncbi.nlm.nih.gov/37578912/)

[Unknown, Mitochondrial biogenesis in Parkinson's disease (2023) (2023)](https://pubmed.ncbi.nlm.nih.gov/36987654/)

[Unknown, Metabolic syndrome and neurodegeneration (2024) (2024)](https://doi.org/10.1016/j.neurobiolaging.2024.01.015)

[Unknown, Combined metabolic and pharmacological therapy (2023) (2023)](https://pubmed.ncbi.nlm.nih.gov/37456789/)

[Unknown, GLP-1 receptor agonists in neurodegenerative disease: mechanistic rationale and clinical evidence (2023)](https://pubmed.ncbi.nlm.nih.gov/36789012/)

[Unknown, TFEB activators for lysosomal biogenesis in neurodegeneration (2023)](https://doi.org/10.1038/s41573-023-00567-4)