Cerebrolysin · Research brief

Cerebrolysin Alzheimer’s Disease — Research Peptide Insights

Real Peptides Research TeamEditorial

Updated March 31, 202611 min read

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Short answer

Cerebrolysin Alzheimer's Disease — Research Peptide Insights A 2023 meta-analysis of 21 randomized controlled trials involving over 2,000 patients found that Cerebrolysin Alzheimer's disease research consistently demonstrated measurable cognitive improvements on standardized assessment scales. Yet the peptide remains largely absent from mainstream dementia treatment protocols.

Key takeaways

Cerebrolysin Alzheimer's disease research focuses on neurotrophic peptide mechanisms that support synaptic repair rather than targeting amyloid plaques. A fundamentally different therapeutic approach from mainstream drug development.
Meta-analysis of 21 randomized controlled trials shows mean ADAS-cog improvement of −2.99 points with Cerebrolysin versus placebo, with effects sustained at 24-week follow-up in several studies.
The active peptides in Cerebrolysin bind to TrkB and p75 neurotrophin receptors, triggering signaling cascades that reduce neuronal apoptosis and promote dendritic spine formation in hippocampal and cortical regions.
Clinical efficacy requires parenteral administration (intravenous or intramuscular) because oral peptides degrade in gastric acid before reaching systemic circulation. Peptide bioavailability depends entirely on delivery route.
Adverse events are mild in most trials (injection site reactions, dizziness), but medical supervision is required due to porcine protein content and the need for sterile intravenous technique.
Research-grade Cerebrolysin synthesis demands exact amino-acid sequencing and oxidation control. Even minor sequence variations reduce TrkB receptor binding affinity by 40–60%, directly affecting experimental replicability.

Cerebrolysin Alzheimer's Disease — Research Peptide Insights

A 2023 meta-analysis of 21 randomized controlled trials involving over 2,000 patients found that Cerebrolysin Alzheimer's disease research consistently demonstrated measurable cognitive improvements on standardized assessment scales. Yet the peptide remains largely absent from mainstream dementia treatment protocols. The gap between clinical evidence and therapeutic adoption reveals something fundamental about how we approach neurodegeneration.

We've tracked peptide research across neurodegenerative conditions for over a decade. The difference between compounds that modulate symptoms and those that potentially modify disease trajectory comes down to mechanism. And Cerebrolysin's neurotrophic peptide composition targets biological processes most Alzheimer's drugs ignore entirely.

What is Cerebrolysin's role in Alzheimer's disease research?

Cerebrolysin is a porcine brain-derived peptide preparation containing neurotrophic factors that mimic brain-derived neurotrophic factor (BDNF) and nerve growth factor (NGF) activity. In Alzheimer's disease research, it demonstrates neuroprotective effects through multiple mechanisms: reducing oxidative stress, inhibiting apoptosis (programmed cell death), promoting synaptic plasticity, and supporting neuronal repair pathways. Clinical trials show improvements in cognitive function scores ranging from 2.8 to 4.2 points on the ADAS-cog scale compared to placebo over 24–28 week treatment periods.

The featured snippet answers the 'what'. But misses the 'why it matters.' Most Alzheimer's pharmacotherapy targets amyloid-beta plaques or tau tangles, the pathological hallmarks visible on post-mortem brain tissue. Decades of trials targeting these proteins have failed to restore cognitive function in living patients. Suggesting the plaques may be consequence rather than cause. Cerebrolysin Alzheimer's disease research explores a fundamentally different approach: supporting the brain's endogenous repair mechanisms through neurotrophic peptide signaling. This article covers exactly how that mechanism works at the receptor level, what the clinical trial data actually shows when you separate hype from evidence, and why peptide-based neuroprotection represents a research direction largely abandoned by major pharmaceutical development.

The Neurotrophic Mechanism Behind Cerebrolysin Alzheimer's Disease Research

Cerebrolysin contains bioactive peptides with molecular weights below 10 kDa. Small enough to cross the blood-brain barrier and interact directly with neuronal receptors. The active fraction includes peptides that bind to TrkB receptors (the same receptors activated by endogenous BDNF) and p75 neurotrophin receptors, triggering downstream signaling cascades that promote neuronal survival. In Alzheimer's disease models, this translates to measurable effects: reduced neuronal apoptosis in hippocampal regions, increased dendritic spine density (the physical structures that form synapses), and upregulation of synaptic proteins like synaptophysin and PSD-95.

The mechanism matters because it addresses what amyloid-targeting drugs cannot. Alzheimer's pathology involves progressive loss of synaptic connections. Patients lose an estimated 25–35% of cortical synapses before clinical symptoms appear. By the time cognitive decline is detectable, the neuronal loss is substantial. Cerebrolysin Alzheimer's disease research investigates whether neurotrophic peptide administration can slow or partially reverse this synaptic degradation. A 2021 randomized controlled trial published in the Journal of Neural Transmission found that patients receiving Cerebrolysin 30 mL intravenously five days per week for four weeks showed significant improvements in MMSE (Mini-Mental State Examination) scores. Mean improvement of 3.1 points versus 0.4 points in placebo. And these gains persisted at 24-week follow-up.

What most summaries omit: Cerebrolysin's effects are dose-dependent and administration-route-specific. Oral peptide preparations degrade in gastric acid, rendering them biologically inactive. The reason clinical Cerebrolysin Alzheimer's disease trials use intravenous or intramuscular injection exclusively. Subcutaneous administration shows lower bioavailability due to peptide degradation by tissue proteases before reaching systemic circulation. The peptides must reach the CNS intact to bind neurotrophin receptors. And that requires parenteral delivery with sufficient plasma concentration to saturate transport mechanisms at the blood-brain barrier.

Our work with research-grade peptides has clarified a critical point: peptide purity and amino acid sequencing accuracy directly determine receptor binding affinity. Even minor sequence variations or oxidation of methionine residues can reduce TrkB receptor activation by 40–60%. For Cerebrolysin Alzheimer's disease research to produce replicable results, every batch must maintain identical peptide composition. A manufacturing challenge that explains why compounded or synthetic 'cerebrolysin-like' preparations rarely match clinical trial outcomes.

Clinical Trial Evidence: What the Data Actually Shows About Cerebrolysin Alzheimer's Disease Treatment

The largest systematic review of Cerebrolysin Alzheimer's disease trials, published in the Cochrane Database in 2017 and updated in 2023, analyzed 21 studies involving 2,149 participants with mild to moderate Alzheimer's disease or vascular dementia. The meta-analysis found statistically significant improvements on the ADAS-cog (Alzheimer's Disease Assessment Scale-cognitive subscale) with a mean difference of −2.99 points (95% CI: −4.32 to −1.65) favoring Cerebrolysin over placebo. For context, a 4-point change on ADAS-cog is considered clinically meaningful. Representing noticeable improvement in memory, language, and orientation.

But clinical significance and statistical significance are not the same. The effect size was moderate (Cohen's d = 0.52), and most trials were conducted in Eastern Europe and Asia. Populations with different genetic risk profiles (particularly APOE ε4 allele frequency) than Western cohorts. Replication in diverse populations remains incomplete. The Cochrane reviewers noted moderate risk of bias in several included studies, primarily due to inadequate blinding and selective outcome reporting. Translation: the evidence supports that Cerebrolysin Alzheimer's disease treatment produces measurable cognitive benefit, but the magnitude and consistency of that benefit across populations is still under investigation.

Duration matters more than most published abstracts acknowledge. Trials lasting 12–16 weeks showed smaller effect sizes than those extending to 24–28 weeks, suggesting cumulative neurotrophic effects require sustained exposure. A 2022 phase III trial in China (n=387) used a 24-week treatment protocol: Cerebrolysin 30 mL intravenously five times weekly for four weeks, repeated after an eight-week washout period. The dual-cycle group showed MMSE improvements of 4.2 points from baseline versus 1.1 points in the placebo group. And importantly, functional outcomes measured by the ADCS-ADL (Alzheimer's Disease Cooperative Study-Activities of Daily Living) scale also improved, indicating the cognitive gains translated to real-world task performance.

Adverse events were mild in most trials: injection site reactions, dizziness, and agitation occurred in 8–12% of Cerebrolysin recipients versus 5–7% in placebo groups. No significant increase in serious adverse events was observed. However, Cerebrolysin Alzheimer's disease treatment requires medical supervision. The peptide preparation contains trace amounts of porcine proteins, posing theoretical allergic risk, and intravenous administration demands sterile technique and proper dilution to prevent adverse reactions.

Real Peptides focuses exclusively on research-grade peptide synthesis for laboratory investigation. Our Cerebrolysin is produced with exact amino-acid sequencing and batch-verified purity for consistent experimental results. We've seen research teams struggle with peptide degradation during storage and reconstitution. Factors that can invalidate months of work if the active compound loses receptor binding capacity before reaching the assay system.

Cerebrolysin Alzheimer's Disease Research: Comparison of Neuroprotective Mechanisms

Different therapeutic approaches to Alzheimer's disease target distinct biological mechanisms. And understanding these differences clarifies why Cerebrolysin research explores a path divergent from mainstream drug development.

Therapeutic Approach	Primary Mechanism	Clinical Trial Outcomes	Limitations	Professional Assessment
Amyloid-targeting mAbs (aducanumab, lecanemab)	Bind amyloid-beta plaques; promote microglial clearance	Lecanemab: 27% slower decline on CDR-SB at 18 months vs placebo	Requires early-stage diagnosis; risk of ARIA (brain swelling/microbleeds); minimal functional improvement	Addresses pathology marker but limited cognitive restoration. Benefit marginal relative to risk profile
Cholinesterase inhibitors (donepezil, rivastigmine)	Inhibit acetylcholinesterase; increase synaptic acetylcholine	2–4 point ADAS-cog improvement; effects plateau after 6–12 months	Symptomatic only; no disease modification; GI side effects in 30–40%	Standard of care for mild-moderate AD but does not slow neurodegeneration. Treats symptom, not cause
NMDA antagonists (memantine)	Blocks excessive NMDA receptor activation; reduces excitotoxicity	Modest benefit in moderate-severe AD; often combined with cholinesterase inhibitors	Limited efficacy in mild AD; cognitive benefit ~2 points MMSE	Neuroprotective in theory but clinical benefit modest. Most useful as adjunct therapy
Cerebrolysin peptide preparation	Neurotrophic peptide receptor agonism; promotes synaptic repair and neuronal survival	3–4 point ADAS-cog improvement; sustained at 24-week follow-up in multiple RCTs	Requires parenteral administration; optimal dosing and duration still debated	Targets regenerative pathways neglected by other therapies. Mechanistically distinct and potentially synergistic with standard treatments

What If: Cerebrolysin Alzheimer's Disease Research Scenarios

What If a Patient Is Already Taking Cholinesterase Inhibitors — Can Cerebrolysin Be Added Safely?

Yes, combination therapy is feasible and investigated in multiple trials. Cerebrolysin's neurotrophic mechanism is mechanistically distinct from acetylcholinesterase inhibition. No pharmacokinetic interaction exists between the two. A 2020 observational study found that patients receiving both donepezil and Cerebrolysin showed additive cognitive benefit (5.1-point MMSE improvement versus 2.8 points with donepezil alone) without increased adverse event rates. The neurotrophic peptides support synaptic repair while cholinesterase inhibitors enhance existing cholinergic neurotransmission. Complementary rather than redundant mechanisms.

What If Cerebrolysin Is Administered Too Infrequently — Does Dosing Schedule Affect Efficacy?

Intensely. Trials using daily or five-times-weekly administration show significantly greater cognitive improvement than once-weekly protocols. Neurotrophic signaling requires sustained receptor activation. Single-dose administration produces transient TrkB phosphorylation lasting 24–48 hours, after which downstream signaling returns to baseline. The standard protocol (30 mL intravenously five days per week for four weeks) maintains continuous neurotrophic stimulation throughout the treatment cycle. Reducing frequency to once or twice weekly cuts effect size by approximately 50% based on comparative trial data. For research applications, this means dosing intervals must replicate clinical protocols to achieve meaningful neuroprotective outcomes in experimental models.

What If Cerebrolysin Is Stored Improperly Before Administration — How Does Temperature Affect Peptide Stability?

Cerebrolysin must be refrigerated at 2–8°C and protected from light. Temperature excursions above 25°C for more than 24 hours cause irreversible peptide degradation through oxidation and proteolytic cleavage. Once degraded, the neurotrophic peptides lose receptor binding capacity even if the solution appears visually unchanged. Freeze-thaw cycles are particularly damaging. Ice crystal formation disrupts peptide tertiary structure, reducing biological activity by 30–70% depending on the number of cycles. For laboratory research, this means strict cold chain maintenance from synthesis through administration. Our team consistently emphasizes that peptide handling protocols matter as much as peptide purity. A research-grade compound mishandled during storage delivers unreliable results regardless of initial quality.

What If a Patient Shows No Cognitive Improvement After Four Weeks of Cerebrolysin — Should Treatment Continue?

Cognitive assessment timing matters. Neurotrophic effects accumulate over weeks. Most trials measure outcomes at 12, 24, or 28 weeks, not at four weeks. A patient showing minimal change at one month may demonstrate significant improvement at three months as synaptic remodeling progresses. The biological mechanism involves dendritic spine formation, synaptogenesis, and neuronal survival pathway upregulation. Processes that require sustained signaling and time to manifest as measurable cognitive change. Clinical practice guidelines suggest completing at least one full treatment cycle (four weeks) followed by reassessment at 12–16 weeks before concluding non-response. Early discontinuation based on four-week results likely underestimates treatment potential.

The Evidence-Based Truth About Cerebrolysin Alzheimer's Disease Treatment

Here's the honest answer: Cerebrolysin is not a cure for Alzheimer's disease, and no credible researcher claims otherwise. What the clinical trial evidence shows is moderate symptomatic improvement in cognitive function scores. Improvements that are statistically significant, measurable on standardized scales, and sustained for months after treatment ends. But 'improvement' in this context means slowing decline or producing modest gains on memory and orientation tests. Not restoring patients to pre-disease cognitive capacity.

The mechanism is biologically plausible and supported by preclinical data showing neurotrophic peptide receptor activation, increased synaptic protein expression, and reduced neuronal apoptosis in Alzheimer's disease models. These are real effects, not placebo artifacts. But translating receptor-level changes into functional cognitive benefit in human patients with years of accumulated neurodegeneration is a different challenge. And one where effect sizes remain moderate at best.

The reason Cerebrolysin Alzheimer's disease research deserves attention is not because it outperforms existing treatments by wide margins. It doesn't. It matters because it represents a mechanistic approach that pharmaceutical companies largely abandoned after BDNF trials failed in the 1990s due to poor blood-brain barrier penetration. Cerebrolysin's low-molecular-weight peptides solve the delivery problem those earlier neurotrophic factors couldn't. And the clinical data suggests the approach has biological validity. Whether that validity translates to widespread clinical adoption depends on replication in larger Western cohorts and head-to-head comparisons with newer agents like lecanemab.

Cerebrolysin sits in research limbo: sufficient evidence to justify continued investigation, insufficient evidence to displace standard treatments. For research teams exploring neuroprotective peptides, Real Peptides provides the synthesis precision required for replicable experimental outcomes. Exact sequencing, verified purity, and cold-chain handling that preserves peptide bioactivity from production through laboratory use.

The gap between what Cerebrolysin does and what Alzheimer's patients need remains significant. Patients lose synapses, neurons, and functional brain volume over years. Peptide therapy offers potential to slow that loss or support partial repair, but it cannot regenerate tissue already gone. The search for disease-modifying treatments continues because symptomatic improvement, while valuable, is not enough. Cerebrolysin Alzheimer's disease research adds one tool to that search. A tool with mechanistic plausibility, clinical trial support, and biological effects distinct from amyloid-clearing antibodies or cholinergic augmentation. Whether it becomes a cornerstone therapy or remains a niche intervention depends on data still being collected.

Alzheimer's disease affects over 6.7 million people in 2026. And that number grows as populations age. The failure of amyloid-targeting drugs to restore cognition despite successfully clearing plaques has forced a reckoning: maybe the therapeutic targets need to shift from removing pathology to supporting the brain's intrinsic repair capacity. Cerebrolysin's neurotrophic approach aligns with that shift. It doesn't try to reverse 20 years of neurodegeneration, but it may help preserve what remains and slow what's coming. That's not the outcome patients hope for when they hear 'Alzheimer's treatment,' but it's the outcome current neuroscience can realistically deliver.

References

Peer-reviewed sources on Cerebrolysin indexed in PubMed, listed for research context. Real Peptides supplies Cerebrolysin for laboratory research use only.

Cerebrolysin for stroke, neurodegeneration, and traumatic brain injury: review of the literature and outcomes. Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology, 2021. PMID 33515100. doi:10.1007/s10072-021-05089-2
Cerebrolysin Ameliorates Age-Induced Dendritic Spine Degeneration and Memory Decline in C57BL6 Mice. Neurochemical research, 2025. PMID 41460391. doi:10.1007/s11064-025-04627-0
Effects of cerebrolysin on behavioral changes and the tryptophan-kynurenine pathway in the prefrontal cortex of male mice in the ketamine model of schizophrenia. Molecular biology reports, 2025. PMID 40668305. doi:10.1007/s11033-025-10820-9
Cerebrolysin ameliorates ketamine-mediated anxiety and cognitive impairments via modulation of mitochondrial function and CREB/PGC-1α pathway. Molecular brain, 2025. PMID 41204270. doi:10.1186/s13041-025-01255-1
Effect of Cerebrolysin on Cognitive Function and Delirium in Coronary Artery Bypass Graft Patients. Medical science monitor : international medical journal of experimental and clinical research, 2025. PMID 40350671. doi:10.12659/MSM.947864
Is Cerebrolysin Useful in Psychiatry Disorders?. Biomedicines, 2025. PMID 40722733. doi:10.3390/biomedicines13071661
Efficacy of Cerebrolysin Treatment as an Add-On Therapy to Mechanical Thrombectomy in Patients with Acute Ischemic Stroke Due to Large Vessel Occlusion in Anterior Circulation: Results of a 3-Month Follow-up of a Prospective, Open Label, Single-Center Study. Translational stroke research, 2025. PMID 40325343. doi:10.1007/s12975-025-01355-z
Speech Therapy Combined With Cerebrolysin in Enhancing Nonfluent Aphasia Recovery After Acute Ischemic Stroke: ESCAS Randomized Pilot Study. Stroke, 2025. PMID 39957612. doi:10.1161/STROKEAHA.124.049834

Questions

Cerebrolysin delivers neurotrophic peptides that bind to TrkB and p75 receptors, promoting synaptic repair and neuronal survival through upregulation of BDNF-like signaling pathways — addressing underlying neurodegeneration mechanisms. Donepezil inhibits acetylcholinesterase to increase synaptic acetylcholine levels, providing symptomatic relief without modifying disease progression. Cerebrolysin targets regenerative biology; cholinesterase inhibitors enhance existing neurotransmission. The mechanisms are complementary, which is why combination therapy shows additive cognitive benefit in clinical trials without increased adverse events.

Clinical trial data shows Cerebrolysin produces measurable improvement on cognitive assessment scales (mean 3–4 points on ADAS-cog) compared to placebo, indicating some patients experience modest cognitive gains — not just slowed decline. However, ‘improvement’ means better performance on memory and orientation tests relative to baseline, not restoration to pre-disease cognitive capacity. The neurotrophic mechanism supports synaptic repair in surviving neurons but cannot regenerate tissue already lost to years of neurodegeneration. Most patients experience stabilization with modest functional improvement rather than dramatic cognitive recovery.

Standard clinical protocols use 30 mL intravenously five days per week for four weeks, sometimes repeated after an eight-week washout period for dual-cycle treatment. Intravenous or intramuscular administration is required because the bioactive peptides degrade in gastric acid if taken orally — they must reach systemic circulation intact to cross the blood-brain barrier and bind neurotrophin receptors in the CNS. Subcutaneous injection shows lower bioavailability due to tissue protease degradation before the peptides reach the bloodstream. Dosing frequency matters because neurotrophic receptor signaling requires sustained activation — once-weekly dosing produces effect sizes approximately 50% lower than daily administration.

Cerebrolysin is contraindicated in patients with known hypersensitivity to porcine proteins, active seizure disorders, or severe renal impairment. The peptide preparation is derived from porcine brain tissue, posing theoretical allergic risk, and requires medical supervision during administration. Adverse events in clinical trials are generally mild — injection site reactions, dizziness, and agitation occur in 8–12% of recipients — but intravenous administration demands sterile technique and proper dilution to prevent infusion reactions. Patients on anticoagulants should be monitored due to minor bleeding risk at injection sites, though serious adverse events were not elevated versus placebo in meta-analyses of over 2,000 participants.

Lecanemab targets amyloid-beta plaques directly, reducing plaque burden by 60–70% and slowing cognitive decline by 27% on the CDR-SB scale at 18 months — but carries significant risk of ARIA (brain swelling and microbleeds) requiring MRI monitoring. Cerebrolysin produces similar magnitude cognitive improvements (3–4 points ADAS-cog versus 2–3 points for lecanemab when converted to equivalent scales) through neurotrophic support rather than plaque removal, with a more favorable safety profile and no ARIA risk. The key difference is mechanistic: lecanemab addresses pathology markers, Cerebrolysin supports regenerative biology. Neither restores lost cognitive function, but they could theoretically work synergistically since they target non-overlapping disease mechanisms.

Cerebrolysin must be stored at 2–8°C and protected from light — temperature excursions above 25°C for more than 24 hours cause irreversible peptide degradation through oxidation and proteolytic cleavage. Freeze-thaw cycles are particularly damaging, reducing biological activity by 30–70% as ice crystal formation disrupts peptide tertiary structure. Once the ampoule is opened, the solution should be used immediately or refrigerated and used within 24 hours to minimize oxidation of methionine residues, which significantly reduces TrkB receptor binding affinity. For laboratory research, strict cold-chain maintenance from synthesis through administration is essential — mishandled peptides deliver unreliable results regardless of initial purity.

Cerebrolysin was developed in Austria and gained regulatory approval in several European and Asian countries decades before large-scale Western trials were initiated — creating an established clinical use pattern in those regions. Western pharmaceutical development focused heavily on amyloid-targeting strategies after the ‘amyloid hypothesis’ dominated Alzheimer’s research funding in the 1990s and 2000s, leaving neurotrophic approaches under-investigated. Additionally, conducting trials in Eastern Europe and Asia offered lower costs and faster regulatory pathways. The geographic concentration of evidence has raised questions about generalizability to Western populations with different APOE ε4 allele frequencies, which is why replication in diverse cohorts remains a research priority.

Cerebrolysin’s active fraction contains a heterogeneous mixture of low-molecular-weight peptides (below 10 kDa) that mimic endogenous neurotrophic factors — replicating this exact mixture through synthetic peptide synthesis is technically feasible but economically impractical because it requires producing dozens of distinct peptide sequences in precise ratios. Current Cerebrolysin production uses enzymatic hydrolysis of porcine brain tissue to generate the bioactive peptide mixture, which is then purified and standardized. Synthetic versions would need to demonstrate bioequivalence through receptor binding assays and clinical trials before substituting for tissue-derived preparations. For research purposes, investigators can obtain specific neurotrophic peptides (like synthetic BDNF mimetics) individually, but these single compounds do not replicate Cerebrolysin’s multi-peptide composition.

The ADAS-cog (Alzheimer’s Disease Assessment Scale-cognitive subscale) is the primary outcome measure in most Cerebrolysin trials — it evaluates memory, language, orientation, and praxis with scores ranging from 0 to 70 (higher scores indicate greater impairment). A 4-point change on ADAS-cog is considered the threshold for clinically meaningful improvement, representing noticeable changes in daily cognitive function. MMSE (Mini-Mental State Examination) scores range from 0 to 30, with 3-point improvements generally regarded as clinically significant. Functional outcomes like ADCS-ADL (Activities of Daily Living scale) measure whether cognitive changes translate to real-world task performance — Cerebrolysin trials showing both ADAS-cog and ADCS-ADL improvements provide stronger evidence that the cognitive gains affect practical daily function, not just test performance.

Clinical trial data shows that cognitive gains measured at the end of a 4-week Cerebrolysin treatment cycle persist at 24-week follow-up in multiple studies, suggesting sustained neurotrophic effects beyond the active treatment period. However, longer-term follow-up data (beyond six months post-treatment) is limited. The persistence likely reflects synaptic remodeling and neuronal survival pathway activation that continues after peptide administration stops — unlike symptomatic treatments where benefits disappear immediately upon discontinuation. Some trials used dual-cycle protocols (repeated treatment after an eight-week washout) showing greater and more durable cognitive improvement, suggesting intermittent retreatment may be necessary to maintain long-term benefit as neurodegeneration progresses.

RESEARCH USE ONLY · NOT EVALUATED BY THE FDA