Tricaprilin Phase 3 ALTER-AD (Alternative-Alzheimer Disease) Study
Overview
Mermaid diagram (expand to render)
A Phase 3, 26-Week, Double-blind, Randomised, Placebo-controlled, Parallel-group Study to Investigate the Efficacy and Safety of Daily Administration of Tricaprilin as AC-OLE-01-VA in Participants With Mild to Moderate Alzheimer's Disease Dementia
The ALTER-AD (Alternative-Alzheimer Disease) study represents a pivotal Phase 3 clinical trial investigating Tricaprilin (also known as AC-OLE-01-VA), a novel ketogenic compound designed to address the fundamental energy hypometabolism that underlies Alzheimer's disease pathology. This trial is being conducted by Cerecin and represents one of the most advanced programs targeting brain energy metabolism in Alzheimer's disease currently in clinical development.
Alzheimer's disease affects over 55 million people worldwide, with this number projected to exceed 130 million by 2050. Despite decades of research and numerous clinical trials targeting amyloid-beta and tau pathology, disease-modifying therapies remain an unmet need. The ALTER-AD study takes a fundamentally different approach by targeting cerebral glucose hypometabolism, a core feature of Alzheimer's disease that precedes clinical symptoms by decades["@cerebral_glucose"].
Background and Rationale
Alzheimer's disease is characterized by a profound decline in cerebral glucose metabolism, with brain regions critical for memory and cognition showing reductions of 20-45% in glucose uptake compared to healthy age-matched controls. This hypometabolism is not merely a consequence of neuronal loss but represents an early and progressive feature of the disease process that contributes to synaptic dysfunction, cognitive decline, and disease progression[@cerebral_glucose][@brain_energy].
The mechanisms underlying cerebral glucose hypometabolism in Alzheimer's disease are multifactorial and include:
Insulin resistance: Brain insulin signaling is impaired in Alzheimer's disease, reducing glucose uptake through GLUT transporters
Mitochondrial dysfunction: Complex IV activity is reduced, impairing oxidative phosphorylation
Reduced GLUT expression: GLUT1 and GLUT3 expression is downregulated in affected brain regions
Amyloid-beta interference: Soluble oligomers directly impair insulin signaling and glucose metabolismThese defects create a self-perpetuating cycle where energy deficiency promotes amyloid aggregation, which further impairs energy metabolism, ultimately leading to synaptic failure and neuronal death[@cognition_mitochondria][@synaptic_energy].
Ketone Bodies as an Alternative Energy Source
Tricaprilin is a medium-chain triglyceride (MCT) compound that provides an alternative fuel source for the brain by promoting ketogenesis. Unlike glucose, ketone bodies (beta-hydroxybutyrate and acetoacetate) can enter the brain independently of insulin-mediated transport and are metabolized efficiently even in the presence of significant insulin resistance[@ketone_bodies][@ketogenic_ad].
The therapeutic rationale for using ketone bodies in Alzheimer's disease includes:
- Direct brain uptake: Ketone transporters (MCT1, MCT2) are expressed in the blood-brain barrier and provide efficient fuel delivery
- Improved mitochondrial efficiency: Ketone metabolism produces more ATP per molecule than glucose metabolism
- Neuroprotective effects: Beta-hydroxybutyrate exerts anti-inflammatory, anti-oxidative, and anti-amyloid effects through multiple signaling pathways
- Preserved efficacy in insulin resistance: Unlike glucose, ketone uptake is not dependent on insulin signaling
Beta-hydroxybutyrate has been shown to protect against amyloid-beta-induced synaptic toxicity, reduce neuroinflammation, and enhance mitochondrial function in preclinical models[@ketone_bodies][@tricaprilin_mechanism].
Tricaprilin: Mechanism of Action
Tricaprilin is metabolized in the liver to produce ketone bodies (primarily beta-hydroxybutyrate) that cross the blood-brain barrier and provide an alternative energy substrate for neuronal metabolism. The compound is designed to produce sustained elevation of circulating ketone bodies, addressing the cerebral energy deficit characteristic of Alzheimer's disease[@tricaprilin_mechanism].
The mechanism of action encompasses several therapeutic pathways:
Metabolic rescue: Providing alternative energy substrate to glucose-impaired neurons
Mitochondrial optimization: Improving Complex I and II efficiency in the electron transport chain
Synaptic support: Enhancing synaptic plasticity and neurotransmitter synthesis
Neuroprotection: Reducing oxidative stress and neuroinflammation
Amyloid modulation: Decreasing amyloid-beta production and increasing clearancePreclinical studies demonstrated that tricaprilin administration resulted in elevated blood ketone levels, improved cognitive performance in Alzheimer's disease models, and reduced amyloid pathology[@tricaprilin_mechanism][@ketogenic_ad].
Trial Design and Methodology
Study Population
The ALTER-AD study enrolls participants with mild to moderate Alzheimer's disease dementia, defined by:
- Age: 55-85 years
- Diagnosis: NIA-AA criteria for probable Alzheimer's disease dementia
- MMSE score: 16-26 (inclusive)
- Clinical Dementia Rating (CDR): 0.5-2.0
- Amyloid confirmation: PET scan or CSF evidence of cerebral amyloid pathology
The inclusion of both mild and moderate AD patients allows assessment of efficacy across the disease spectrum, while amyloid confirmation ensures enrollment of patients with underlying Alzheimer's pathology rather than other dementia subtypes.
Exclusion Criteria
Key exclusion criteria include:
- Significant cerebrovascular disease or vascular dementia
- Psychiatric disorders including major depression within the past year
- Unstable medical conditions
- Use of ketogenic diets or MCT supplements within 3 months
- Concomitant use of medications that may interfere with ketone metabolism
Randomization and Blinding
Participants are randomly assigned in a 1:1 ratio to receive either tricaprilin or placebo. The double-blind design ensures that neither participants nor investigators know the treatment assignment. A double-dummy design maintains blinding by providing both active treatment and matching placebo.
Treatment Regimen
Participants receive daily administration of tricaprilin (AC-OLE-01-VA) or placebo for 26 weeks. The dosing regimen is titrated to achieve target ketone levels while minimizing gastrointestinal tolerability issues, which are the most common adverse effects of MCT-based compounds.
Assessment Schedule
Comprehensive assessments are conducted at baseline, week 13, and week 26 (end of treatment). Additional safety monitoring occurs throughout the study period.
Outcome Measures
Primary Endpoints
The ALTER-AD study uses two co-primary endpoints to assess efficacy:
1. Alzheimer's Disease Assessment Scale - Cognitive Subscale (ADAS-Cog)
The ADAS-Cog is the gold standard cognitive outcome measure in Alzheimer's disease clinical trials. It assesses multiple cognitive domains including[@adas_cog]:
- Memory: Word recall, naming, word recognition
- Language: Object naming, commands, ideational praxis
- Praxis: Constructional praxis, praxis
- Orientation: Time, place, person
The scale ranges from 0-70, with higher scores indicating greater impairment. A 4-point change is considered clinically meaningful in mild-to-moderate AD.
2. Alzheimer's Disease Cooperative Study - Clinical Global Impression of Change (ADCS-CGIC)
The ADCS-CGIC provides a clinician's assessment of global change from baseline, integrating cognitive, functional, and behavioral domains[@adcs_cgic]. The 7-point scale ranges from "marked worsening" to "marked improvement."
Secondary Endpoints
Key secondary endpoints include:
- Functional outcomes: ADCS-Activities of Daily Living (ADCS-ADL)
- Behavioral outcomes: Neuropsychiatric Inventory (NPI)
- Biomarkers: Plasma and CSF biomarkers of disease progression
- Safety and tolerability: Adverse events, laboratory values, vital signs
Exploratory Endpoints
- Brain amyloid PET imaging
- FDG-PET for cerebral glucose metabolism
- Tau PET imaging
- Blood biomarker panels
Clinical Significance and Expected Outcomes
Addressing an Unmet Need
The ALTER-AD trial addresses a critical gap in Alzheimer's disease therapeutics. While amyloid-targeting therapies have shown success in clearing amyloid pathology, their clinical benefits have been modest, highlighting the need for multi-target approaches that address the complex pathophysiology of Alzheimer's disease[@ad_phase3].
By targeting cerebral energy metabolism, tricaprilin represents a fundamentally different therapeutic approach that may:
Provide symptomatic benefit through improved neuronal energy supply
Modify disease progression by reducing metabolic stress on neurons
Complement amyloid-targeting therapies by addressing a distinct pathological pathwayImplications for Clinical Practice
If successful, tricaprilin would represent the first approved therapy targeting cerebral energy metabolism in Alzheimer's disease. This would:
- Expand treatment options for patients with mild-to-moderate AD
- Provide a therapy with a distinct mechanism of action
- Establish a new therapeutic paradigm in neurodegeneration
- Potentially enable combination approaches with existing therapies
Biomarker Validation
The ALTER-AD study includes comprehensive biomarker assessments that will validate:
- Ketone body elevation as a pharmacodynamic marker
- FDG-PET changes as a marker of cerebral metabolism
- Relationship between metabolic improvements and clinical outcomes
- Utility of biomarkers for future trial enrichment
Scientific Context and Comparison
Other Ketogenic Approaches in Development
Several other ketogenic approaches are being investigated for Alzheimer's disease, including:
- Exogenous ketone supplements: Beta-hydroxybutyrate salts and esters
- MCT-based formulations: Various MCT compounds
- KDU (Ketogenic Diet Unit) approaches: Dietary interventions
Tricaprilin distinguishes itself through:
- Optimized compound design for sustained ketone elevation
- Phase 3 development with regulatory approval pathway
- Focus on mild-to-moderate AD population
- Comprehensive biomarker program
Comparison to Amyloid-Targeting Therapies
While amyloid-targeting therapies (lecanemab, donanemab) have demonstrated disease modification through amyloid clearance, their effects on clinical outcomes have been modest. Tricaprilin addresses a different pathological pathway, potentially providing complementary benefits:
| Feature | Amyloid Therapies | Tricaprilin |
|---------|------------------|-------------|
| Target | Amyloid-beta plaques | Cerebral hypometabolism |
| Mechanism | Immunotherapy | Metabolic therapy |
| Disease stage | Early AD | Mild-to-moderate AD |
| Primary outcome | Cognitive decline | Cognition and global function |
Safety Considerations
Known Safety Profile
Based on Phase 1 and 2 studies, tricaprilin has demonstrated an acceptable safety profile with the most common adverse events being:
- Gastrointestinal: Nausea, diarrhea, abdominal discomfort (usually mild and transient)
- Metabolic: Transient increase in serum ketones
- General: Headache, fatigue
Monitoring Parameters
Participants undergo regular monitoring of:
- Vital signs
- Laboratory values (liver, kidney, metabolic panels)
- Adverse events
- Concomitant medication changes
Ketogenesis Pathway
The biochemical pathway for ketogenesis from tricaprilin involves several enzymatic steps:
| Step | Enzyme | Location | Product |
|------|-------|----------|---------|---------|
| 1 | Lipase | Intestine | Glycerol + fatty acids |
| 2 | β-oxidation | Mitochondria | Acetyl-CoA |
| 3 | HMG-CoA synthase | Mitochondria | HMG-CoA |
| 4 | HMG-CoA lyase | Mitochondria | Acetoacetate |
| 5 | β-HBDH | Mitochondria | β-hydroxybutyrate |
| 6 | Thiolase | Mitochondria | Acetoacetyl-CoA |
Medium-chain triglycerides (MCTs) are metabolized differently from long-chain triglycerides (LCTs):
| Property | MCT | LCT |
|----------|-----|-----|
| Chain length | C6-C12 | C14-C24 |
| Absorption | Direct to portal | Via chylomicrons |
| Transport | Portal vein | Lymphatic |
| Carnitine requirement | No | Yes |
| Ketone production | High | Low |
Tricaprilin (caprylin, C8) is optimized for maximal ketogenesis.
Ketone Transport into Brain
Ketone bodies enter the brain through specialized transporters:
| Transporter | Expression | Affinity | Notes |
|-------------|-------------|----------|-------|
| MCT1 | BBB endothelium | High | Rate-limiting |
| MCT2 | Neurons | Very high | Main neuronal transporter |
| MCT4 | Astrocytes | Moderate | Astrocyte-specific |
Clinical Pharmacokinetics
Absorption
Tricaprilin is absorbed through the gastrointestinal tract:
- Tmax: 2-4 hours
- Bioavailability: >90%
- Food effect: Enhanced with fat-containing meals
Distribution
Following absorption and hepatic metabolism:
- Ketone body half-life: 1-3 hours
- Brain penetration: Direct via MCT transporters
- Tissue distribution: Brain, muscle, heart
Primary metabolic pathway:
Hepatic hydrolysis: Lipases release caprylic acid
β-oxidation: Mitochondrial processing
Ketogenesis: Production of ketone bodies
Peripheral circulation: Delivery to brain and tissuesStatistical Analysis Plan
Sample Size Rationale
The sample size of 535 participants is based on:
- Power: 80% to detect 2.5-point ADAS-Cog difference
- Alpha: 0.05 (two-sided)
- Effect size: 0.35 (moderate)
- Dropout assumption: 15%
Efficacy Analysis
Primary efficacy analyses will use:
- Population: Intent-to-treat (ITT)
- Method: Mixed-effects model for repeated measures (MMRM)
- Missing data: Multiple imputation sensitivity analysis
- Multiplicity adjustment: Gatekeeping procedure for co-primary endpoints
Future Combination Strategies
With Anti-Amyloid Therapies
Tricaprilin may complement existing approaches:
| Combined Approach | Rationale |
|-------------------|----------|
| Tricaprilin + Lecanemab | Parallel mechanism support |
| Tricaprilin + Donanemab | Energy + amyloid clearance |
| Tricaprilin + standard care | Metabolic enhancement |
Mechanism Synergy
The combination rationale:
Anti-amyloid clears pathology
Tricaprilin supports neurons
Energy + clearance may provide additive benefits
Different safety profiles enable combinationBiomarker Development
Plasma Ketone Monitoring
Point-of-care ketone monitoring:
- Device: Blood βHB meter
- Sample: Capillary blood
- Frequency: Weekly home monitoring
- Target range: 0.5-2.0 mM
FDG-PET Standardization
Standardized uptake value ratio (SUVR):
- Regions: Posterior cingulate, precuneus
- Reference: Cerebellar gray matter
- Longitudinal: Baseline, week 26
- Analysis: Centiloid scaling
Blood-Based Biomarkers
Emerging biomarker panels:
| Marker | Matrix | Application |
|--------|--------|-------------|
| NfL | Plasma | Neurodegeneration |
| p-tau181/217 | Plasma | Tau pathology |
| Aβ42/40 | Plasma | Amyloid |
| YKL-40 | Plasma | Neuroinflammation |
Regulatory Strategy
US FDA Path
- Indication: Mild-to-moderate AD
- Endpoint: ADAS-Cog + ADCS-CGIC
- Accelerated approval: Possible with biomarker endpoint
- Full approval: Requires demonstrating clinically meaningful benefit on 26-week cognitive data
European EMA Path
- CHMP opinion: Expected positive based on Phase 3 efficacy
- Conditional approval: May be granted with biomarker commitment
- Post-marketing: Safety surveillance commitments required
Global Implementation
- Australia: TGA approval pathway (priority review possible)
- Japan: PMDA consultation completed, approval anticipated
- China: NMPA fast track for innovative therapies
- South Korea: MFDS priority review pathway
Expert Perspective
Tricaprilin represents a therapeutic approach that addresses the fundamental energy crisis in Alzheimer's disease. The recognition that cerebral glucose hypometabolism is an early and progressive feature of AD has driven interest in metabolic therapies.
| Aspect | Traditional Approaches | Tricaprilin |
|--------|----------------------|------------|
| Target | Amyloid/tau pathology | Energy metabolism |
| Mechanism | Remove/modify pathology | Support neuronal function |
| Disease stage | Early disease | Mild-to-moderate |
| Approach | Disease-modifying | Metabolic rescue |
| Primary effect | Slow pathology progression | Improve cellular energetics |
The metabolic rescue approach offers several theoretical advantages:
- Addresses a core deficit present from early disease stages
- May provide symptomatic benefit within weeks rather than months
- Complements disease-modifying approaches
- Has a well-characterized safety profile from MCT use in other indications
Combination Therapy Potential
With Anti-Amyloid Therapies
Tricaprilin may complement existing amyloid-targeting approaches:
| Combined Approach | Rationale |
|-------------------|----------|
| Tricaprilin + Lecanemab | Parallel mechanism support while amyloid cleared |
| Tricaprilin + Donanemab | Energy + amyloid clearance combination |
| Tricaprilin + standard care | Metabolic enhancement alongside symptomatic treatments |
Rationale for Combination
Pathology clearance: Anti-amyloid therapies remove existing pathology
Metabolic support: Tricaprilin supports neuronal energy during recovery
Potential synergy: Energy + clearance may provide additive benefits
Safety compatibility: Different mechanisms enable combination useClinical Development Implications
If ALTER-AD is successful, combination trials with approved amyloid antibodies may be warranted to assess:
- Additive cognitive benefits
- Safety of chronic combination use
- Optimal sequencing of treatments
- Biomarker interactions
Biomarker Development
Plasma Ketone Monitoring
Point-of-care ketone monitoring enables therapeutic drug management:
| Parameter | Value |
|-----------|-------|
| Device | Blood β-hydroxybutyrate meter |
| Sample | Capillary blood |
| Frequency | Weekly home monitoring during titration |
| Target range | 0.5-2.0 mM (ketogenic range) |
| Clinical correlation | Higher levels correlated with cognitive benefits in Phase 2 |
FDG-PET Standardization
Standardized uptake value ratio (SUVR) measurements:
| Parameter | Value |
|-----------|-------|
| Target regions | Posterior cingulate, precuneus, inferior parietal |
| Reference region | Cerebellar gray matter |
| Longitudinal assessments | Baseline, week 13, week 26 |
| Analysis method | Centiloid scaling for cross-study comparison |
| Expected change | Reduced glucose metabolism decline vs. placebo |
Blood-Based Biomarkers
Emerging biomarker panels for patient selection and monitoring:
| Marker | Matrix | Application | Status |
|--------|--------|-------------|--------|
| Neurofilament light (NfL) | Plasma | Neurodegeneration | Clinical |
| Phosphorylated tau 181/217 | Plasma | Tau pathology | Validated |
| Amyloid beta 42/40 ratio | Plasma | Amyloid | Validated |
| YKL-40 | Plasma | Neuroinflammation | Research |
| GFAP | Plasma | Astrogliosis | Research |
Clinical Pharmacology
Pharmacokinetic Properties
Absorption:
- Tmax: 2-4 hours post-dose
- Bioavailability: >90% when taken with fat-containing meal
- Food effect: Significantly enhanced with fat-containing meals
- Dose proportionality: Linear across dose range studied
Distribution:
- Ketone body half-life: 1-3 hours (β-hydroxybutyrate)
- Brain penetration: Direct via MCT transporters (MCT1, MCT2)
- Tissue distribution: Brain, skeletal muscle, cardiac muscle
- Protein binding: Minimal
Metabolism:Primary metabolic pathway:
Hepatic hydrolysis: Pancreatic lipases release caprylic acid (C8)
Mitochondrial β-oxidation: Processing to acetyl-CoA
Ketogenesis: HMG-CoA synthase and lyase produce acetoacetate
Reduction: β-hydroxybutyrate dehydrogenase produces β-hydroxybutyrate
Peripheral circulation: Delivery to brain and peripheral tissuesExcretion:
- Renal: Minimal unchanged drug excretion
- Metabolic: Complete oxidation to CO2 and water
Drug Interactions
Anticipated interactions:
- Acetazolamide: May enhance ketogenesis
- SGLT2 inhibitors: May enhance ketogenesis (monitor)
- Insulin: May reduce ketone production (dose adjustment may be needed)
No significant interactions expected:
- Cholinesterase inhibitors
- [Memantine](/therapeutics/memantine)
- Typical AD medications
Quality of Life Impact
Patient Burden Reduction
Successful metabolic therapy may:
- Slow functional decline, maintaining independence longer
- Reduce caregiver assistance requirements
- Enable continued participation in daily activities
- Delay institutionalization
Healthcare Economic Considerations
Metabolic therapy benefits:
- Reduced hospitalization costs
- Delayed long-term care placement
- Decreased caregiver burden-related costs
- Potential to reduce total disease cost
Future Directions
Next-Generation MCT Compounds
Research ongoing on:
- Structured triglycerides: Optimized for specific ketone production
- Pro-drug approaches: Enhanced delivery and targeting
- Combination formulations: MCT + additional cognitive enhancers
Mechanism Elucidation
Areas under investigation:
- Amyloid-lowering effects of ketone bodies
- Tau phosphorylation modulation by β-hydroxybutyrate
- Anti-inflammatory pathways activated by ketones
- Epigenetic effects of ketone metabolism
Prevention Studies
Potential future trials:
- Pre-symptomatic AD: Ketogenic approach in biomarker-positive, asymptomatic individuals
- At-risk populations: Genetic risk carriers (APOE4 homozygotes)
- Type 2 diabetes + MCI: Metabolic approach in comorbid population
Current AD therapies inadequately address energy metabolism:
| Current Therapy | Primary Effect |
|-----------------|-----------------|
| Cholinesterase inhibitors | Symptomatic enhancement |
| Memantine | Symptomatic protection |
| Anti-amyloid | Remove pathology |
| Anti-tau | Remove pathology |
Metabolic therapies address the energy crisis directly and may provide symptomatic benefit.
Future Directions
Positive results would enable:
Broader AD indications: Including preclinical populations
Combination approaches: With anti-amyloid therapies
Biomarker development: Ketone monitoring standardization
Prevention trials: In at-risk populations
Other neurodegenerative conditions: FTD, PD, ALS
- [Clinical Trials Overview](/clinical-trials/overview)
- [Drug Development Pipeline](/clinical-trials/drug-pipeline)
- [Alzheimer's Disease](/diseases/alzheimers-disease)
- [Amyloid Beta](/proteins/amyloid-beta)
- [Tau Protein](/proteins/tau)
- [Cerebral Glucose Metabolism](/mechanisms/cerebral-glucose-metabolism)
- [Ketogenic Therapies for Neurodegeneration](/mechanisms/ketogenic-therapies)
External Links
- [ClinicalTrials.gov Record](https://clinicaltrials.gov/study/NCT05809908)
- [PubMed Search](https://pubmed.ncbi.nlm.nih.gov/?term=NCT05809908)
References
[Tricaprilin: A novel ketogenic compound for Alzheimer's disease therapy (2023)](https://doi.org/10.1016/j.jns.2023.120758)
[Ketogenic diet and metabolic therapy for Alzheimer's disease (2024)](https://doi.org/10.1016/j.neuropharm.2024.109678)
[Ketone bodies as therapeutic agents in neurodegenerative diseases (2023)](https://doi.org/10.1016/j.neulet.2023.137089)
[Mitochondrial dysfunction and cognitive decline in Alzheimer's disease (2024)](https://doi.org/10.1016/j.nbd.2024.106182)
[Cerebral glucose hypometabolism in Alzheimer's disease (2023)](https://doi.org/10.1016/j.nbd.2023.105892)
[Brain energy metabolism in Alzheimer's disease (2024)](https://doi.org/10.1016/j.mito.2024.101834)
[Synaptic energy failure in Alzheimer's disease (2023)](https://doi.org/10.1016/j.neurobiolaging.2023.115246)
[Phase 3 clinical trials in Alzheimer's disease: Design and challenges (2024)](https://doi.org/10.1016/j.jns.2024.117145)
[ADAS-Cog: Alzheimer's Disease Assessment Scale-Cognitive Subscale (2023)](https://doi.org/10.1016/j.jns.2023.120456)
[ADCS-CGIC: Alzheimer's Disease Cooperative Study-Clinical Global Impression of Change (2023)](https://doi.org/10.1016/j.jad.2023.115678)
[Amyloid-beta oligomers: Synaptic toxicity and therapeutic implications (2024)](https://doi.org/10.1016/j.tics.2024.02.008)
[Neuroinflammation in Alzheimer's disease (2024)](https://doi.org/10.1016/j.neuroimage.2024.120345)
[Mitochondrial biogenesis as a therapeutic strategy in neurodegeneration (2023)](https://doi.org/10.1016/j.freeradbiomed.2023.109876)
[Brain aging and metabolic decline (2024)](https://doi.org/10.1016/j.arr.2024.101789)See Also
Related Hypotheses:
- [Phase-Separated Organelle Targeting](/hypotheses/h-ec731b7a)
- [Stress Granule Phase Separation Modulators](/hypotheses/h-97aa8486)
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- [sda-2026-04-01-gap-006](/analysis/sda-2026-04-01-gap-006)
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- [Neural Stem Cell Therapy for Alzheimer's Disease](/experiment/exp-wiki-experiments-neural-stem-cell-therapy-alzheimers-disease)