Peptides for Memory & Age-Related Cognitive Decline

Your brain starts shrinking in your 30s. By 60, the hippocampus — the region most responsible for forming new memories — is losing roughly 1-2% of its volume per year [1]. Brain-derived neurotrophic factor (BDNF), the protein that keeps synapses healthy and supports memory formation, declines steadily throughout adulthood [2]. Long-term potentiation, the cellular mechanism behind learning, becomes harder to trigger and maintain [3].

None of this is disease. It's normal aging. But normal doesn't mean inevitable or untreatable.

The peptide therapeutics field has produced several compounds that target the specific biological mechanisms driving age-related memory loss — BDNF signaling, synaptic plasticity, mitochondrial function, and neuroinflammation. Some have human clinical trial data. Most are still in preclinical stages. All of them address the underlying biology in ways that existing Alzheimer's drugs and cognitive supplements largely do not.

This guide covers the peptides with the strongest research behind them, organized by the biological mechanism they target, with an honest assessment of where the science actually stands.

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Table of Contents

• Why Memory Declines with Age
• Neurotrophic Peptides: Rebuilding BDNF Signaling
  • Semax
  • Cerebrolysin
  • Dihexa
  • PE-22-28
  • Davunetide (NAP)
• Mitochondrial Peptides: Powering the Aging Brain
  • Humanin
  • MOTS-c
  • SS-31 (Elamipretide)
• Modulatory Peptides: Supporting Memory Through Multiple Pathways
  • Selank
  • BPC-157
  • Pinealon
• Peptide Comparison Table
• What About Alzheimer's Disease?
• Practical Considerations
• FAQ
• The Bottom Line
• References

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Why Memory Declines with Age

Before diving into peptides, it helps to understand what actually goes wrong in the aging brain. Memory loss is not a single problem — it's the downstream result of several interconnected biological changes.

BDNF Decline

BDNF is the brain's primary growth and maintenance factor for neurons. It's especially concentrated in the hippocampus, where it supports synaptic plasticity, neurogenesis, and long-term potentiation (LTP) — the cellular process that encodes memories [2].

Serum and plasma BDNF levels drop with age. In a study published in the Journal of Neuroscience, researchers found that lower BDNF levels correlated with both reduced hippocampal volume and worse memory performance [2]. Genetic studies have identified a single-nucleotide polymorphism on the BDNF gene (Val66Met) that moderates the rate of age-related cognitive decline over a 10-year period [2].

When BDNF drops, synapses weaken, spine density decreases, and the hippocampus shrinks. Memory suffers.

Synaptic Plasticity Shifts

The aging brain doesn't just lose synaptic strength — it changes how synapses operate. NMDA-receptor-dependent LTP, the standard memory-encoding mechanism, becomes harder to induce and maintain. Some aged animals compensate by shifting to NMDA-receptor-independent pathways, and those that make this shift successfully perform better cognitively [3].

Meanwhile, the balance between proBDNF (which promotes apoptosis through p75 receptors) and mature BDNF (which supports survival through TrkB receptors) tips toward proBDNF in aged tissue — meaning the brain is simultaneously losing its growth signal while increasing its pruning signal [3].

Mitochondrial Dysfunction

The brain consumes roughly 20% of the body's energy despite making up only 2% of its weight. When mitochondria — the cellular power plants — become less efficient with age, neurons are among the first cells to suffer. Declining mitochondrial function leads to increased oxidative stress, reduced ATP production, and greater vulnerability to excitotoxicity [4].

This is why mitochondrial-derived peptides like Humanin and MOTS-c have attracted so much attention in aging research.

Neuroinflammation

Chronic, low-grade inflammation in the brain — sometimes called "inflammaging" — increases with age and contributes to synaptic damage, neuronal loss, and impaired memory formation. Activated microglia and elevated pro-inflammatory cytokines create a hostile environment for new learning [5].

Each of these mechanisms represents a potential intervention point. The peptides below target one or more of them.

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Neurotrophic Peptides: Rebuilding BDNF Signaling

These peptides directly address the BDNF decline that underlies much of age-related memory loss.

Semax

Semax is a heptapeptide analog of ACTH(4-10) that has been used clinically in Russia since the 1990s for stroke recovery and cognitive disorders. Its effects on memory are among the best-documented of any nootropic peptide.

BDNF/TrkB activation: A single intranasal dose of Semax (50 mcg/kg) produced a 1.4-fold increase in hippocampal BDNF protein, a 1.6-fold increase in TrkB receptor phosphorylation, and a 3-fold increase in BDNF mRNA in rats [6]. Follow-up studies showed these changes are rapid — beginning within 20 minutes — and region-specific, with different temporal patterns in the hippocampus, frontal cortex, and retina [7].

Neurotrophin activation after brain injury: In a rat model of permanent middle cerebral artery occlusion (stroke), Semax activated transcription of BDNF, TrkC, TrkA, NT-3, and NGF across different time windows (3-72 hours post-occlusion) [8]. This multi-neurotrophin response is relevant to age-related cognitive decline, where multiple neurotrophic pathways are simultaneously compromised.

Memory enhancement in animals: Semax-treated rats showed increased conditioned avoidance reactions — a standard behavioral measure of learning and memory [6].

Human data: In healthy volunteers, Semax at 250-1000 mcg/kg improved attention and short-term memory. Resting-state fMRI confirmed increased activity in the medial frontal cortex, a key node in memory and attention networks [6].

Where it stands: Semax has the strongest combined profile of neurotrophic activity and human cognitive data among nootropic peptides, but it lacks the large-scale clinical trials required for Western regulatory approval.

Cerebrolysin

Cerebrolysin is not a single peptide but a mixture of peptides and amino acids derived from pig brain tissue. It acts as a multitarget peptidergic drug with a neurotrophic mode of action, and it's the only peptide-based compound in this guide with meta-analytic evidence from randomized controlled trials in Alzheimer's disease.

Clinical trial evidence: A 2015 meta-analysis of six randomized controlled trials found that Cerebrolysin was significantly more effective than placebo for cognitive function at 4 weeks (SMD -0.40; p = 0.003) and global clinical change at both 4 weeks (OR 3.32; p = 0.02) and 6 months (OR 4.98; p = 0.015) in patients with mild-to-moderate Alzheimer's disease [9].

Individual trials have shown:

• Significant improvements on the CIBIC+ global assessment scale that persisted two months after treatment ended [10]
• Significant effects on functional and cognitive decline with 30 mL doses [9]
• Potential to prolong the efficacy of cholinesterase inhibitors when used in combination [9]

Mechanism: Cerebrolysin mimics the activity of endogenous neurotrophic factors, supporting neuronal survival, synaptic repair, and neuroplasticity. Its peptide composition allows it to cross the blood-brain barrier [9].

Limitations: Effects are modest compared to currently approved Alzheimer's drugs. Some individual trials found non-significant results. Cerebrolysin requires intravenous administration, is not FDA-approved, and is unavailable in the United States. The evidence for preventing cognitive decline in healthy older adults is essentially nonexistent — nearly all trials have been conducted in people with existing dementia [9].

Dihexa

Dihexa works through the HGF/c-Met pathway to stimulate synaptogenesis — the formation of new synaptic connections. In preclinical models, it has been described as seven orders of magnitude more potent than BDNF at promoting new neural connections in cell culture [11].

Memory effects in animals: Dihexa reversed scopolamine-induced memory impairment and improved spatial learning in aged rats. Its oral bioavailability and blood-brain barrier penetration make it technically attractive as a potential therapeutic [11].

Why it matters for aging: Age-related cognitive decline involves progressive loss of synaptic density. A compound that can stimulate synaptogenesis could theoretically rebuild the connections that aging erodes. This would address a root cause rather than just managing symptoms.

Serious caveats: No human trials exist. The HGF/c-Met pathway is involved in cell growth and tissue repair, but chronic activation raises cancer concerns. Dihexa remains a research-only compound with a fundamentally uncertain safety profile [11].

For more on Dihexa's mechanisms and risks, see our Dihexa cognitive peptide research profile.

PE-22-28

PE-22-28 (Mini-Spadin) blocks TREK-1 potassium channels, which depolarizes neurons and triggers rapid hippocampal neurogenesis and BDNF upregulation. In mice, it approximately doubled the rate of new cell formation in the hippocampus within days [12].

Memory relevance: PE-22-28 activates CREB, a transcription factor critical for memory formation and spatial navigation. The hippocampus — where PE-22-28 concentrates its effects — is the brain region most vulnerable to age-related shrinkage and most critical for new memory encoding [12].

Speed: Where conventional BDNF-boosting strategies take weeks, PE-22-28 produces measurable neurogenic effects within 4 days. This rapid onset sets it apart from other peptides in this category [12].

Limitations: Preclinical only. No human studies. No FDA approval. Its role in age-related cognitive decline remains theoretical.

Davunetide (NAP)

Davunetide is an eight-amino-acid peptide (NAPVSIPQ) derived from activity-dependent neurotrophic protein (ADNP). It stabilizes microtubules and prevents tau pathology — both relevant to age-related neurodegeneration.

Clinical trial results: In a double-blind, placebo-controlled trial in amnestic mild cognitive impairment (a precursor to Alzheimer's), intranasal davunetide at 5 mg/day and 15 mg/twice daily showed dose-dependent cognitive improvements, with sex-specific response patterns [13].

A phase 2/3 trial in progressive supranuclear palsy (a tauopathy) initially showed no overall benefit. However, a sex-dependent reanalysis revealed that davunetide significantly slowed disease progression in women, including protection of brain volume and clinical outcomes [14].

Where it stands: Davunetide is one of the few nootropic peptides to have reached phase 2/3 clinical trials. The sex-dependent efficacy findings — not appreciated in the original analyses — represent an important lesson for future peptide trials. Its FDA status is currently inactive for most indications but listed as Phase 3 for autism spectrum disorder [13].

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Mitochondrial Peptides: Powering the Aging Brain

Mitochondrial dysfunction is a hallmark of brain aging. These peptides target it directly.

Humanin

Humanin is a 24-amino-acid peptide encoded by mitochondrial DNA — specifically the 16S rRNA gene. It was originally discovered in a relatively intact brain region of a postmortem Alzheimer's patient, where it appeared to protect neurons against amyloid beta toxicity [15].

Cognitive aging evidence:

• Humanin administration improved cognition in aged mice [15]
• A genetic variant (rs2854128) in the humanin-coding region is associated with decreased circulating humanin levels and accelerated cognitive aging in a large cohort of older adults [15]
• In rat models, humanin released from astrocytes regulated synaptic plasticity associated with cognitive function [15]
• A humanin derivative (S14G-HN) blocked diazepam-induced cognitive impairment in mice [15]
• Humanin increased dendritic complexity, synaptic protein levels, and synaptic plasticity in amyloid-beta-injected rats [15]

The aging connection: Humanin levels decline with age across multiple species. But in naked mole-rats — animals known for negligible senescence — humanin levels remain remarkably stable throughout their long lifespans. Children of centenarians have significantly higher circulating humanin levels than age-matched controls [15].

Even low-dose humanin treatment in middle-aged mice improved several healthspan markers, including metabolism, fibrosis, and cognitive decline [15].

Limitations: Humanin has not been tested as a therapeutic agent in humans, despite being explored for Alzheimer's disease since its discovery. Delivery and stability challenges remain significant.

MOTS-c

MOTS-c is a 16-amino-acid peptide encoded by the mitochondrial 12S rRNA gene. It activates the AMPK pathway and regulates cellular energy metabolism, insulin sensitivity, and inflammatory responses [16].

Cognitive relevance: MOTS-c was initially thought to have no cognitive effects, but recent research suggests it may support the formation of object and location memory [16]. Its primary mechanisms — reducing inflammation, improving cellular energetics, and countering metabolic dysfunction — address several pathways implicated in age-related cognitive decline.

Significant limitation: MOTS-c does not appear to cross the blood-brain barrier effectively. At doses that improved physical capacity in mice, peripherally administered MOTS-c had no measurable effect on cognition [16]. Its cognitive benefits, if any, may depend on systemic metabolic improvements rather than direct brain effects.

Genetic variants: 5-10% of people with East Asian ancestry carry a MOTS-c variant (MT-1382) associated with increased type 2 diabetes risk, suggesting the peptide's metabolic functions have real physiological consequences [16].

For more on mitochondrial peptides and aging, see our guide on best peptides for anti-aging and longevity.

SS-31 (Elamipretide)

SS-31 is a synthetic tetrapeptide that targets cardiolipin, a phospholipid in the inner mitochondrial membrane. By stabilizing cardiolipin, SS-31 optimizes electron transport chain function, reduces oxidative stress, and improves mitochondrial energy output [17].

Brain aging evidence:

• In neuroinflammation models, SS-31 reversed LPS-induced learning and memory impairment, restored BDNF signaling, normalized synaptic protein levels, and increased synaptic structural complexity [17]
• SS-31 rescued neurovascular coupling responses and improved cognition in aged mice [17]
• The peptide reduces oxidative damage in brain tissue, which is especially significant because the brain generates high levels of reactive oxygen species (ROS) but has relatively weak antioxidant defenses [17]

Age-specificity: Importantly, SS-31 has no measurable effect on mitochondrial function in young, healthy tissue. It only increases ATP production and reduces oxidative stress in aged mitochondria — suggesting it corrects dysfunction rather than overstimulating normal processes [17].

Limitations: Brain concentrations are low compared to plasma, though it does cross the blood-brain barrier. Its neuroprotective effects have not been confirmed in humans. Clinical trials in heart failure and mitochondrial myopathy have produced disappointing results, raising questions about clinical translatability [17].

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Modulatory Peptides: Supporting Memory Through Multiple Pathways

These peptides don't fit neatly into the neurotrophic or mitochondrial categories. They support memory through broader mechanisms — anxiety reduction, neurotransmitter modulation, anti-inflammatory effects, and gut-brain signaling.

Selank

Selank is a tuftsin-derived heptapeptide with both anxiolytic and nootropic properties. For age-related memory, its value lies in addressing the stress-cognition connection.

Chronic stress and anxiety impair hippocampal function and accelerate age-related memory decline. Elevated cortisol levels are directly toxic to hippocampal neurons. By modulating GABA receptors, increasing serotonin and dopamine availability, and reducing neuroinflammation, Selank can reduce the cognitive burden of chronic stress [18].

In animal studies, Selank improved learning, memory formation, and attention — especially under stressful conditions. It also upregulates BDNF and supports synaptic plasticity [18]. For older adults where stress and anxiety compound normal age-related cognitive changes, this dual-action profile is particularly relevant.

For a deeper look at anxiety-focused peptides, see our guide on best peptides for anxiety and stress.

BPC-157

BPC-157 is a gastric pentadecapeptide with documented neuroprotective effects that operate partly through the gut-brain axis.

Memory-relevant mechanisms:

• Protects somatosensory neurons and promotes peripheral nerve regeneration [19]
• Counteracts stroke-induced brain damage: when given during reperfusion after bilateral carotid artery clamping, BPC-157 resolved sustained neuronal damage and restored disturbed memory, locomotion, and coordination in rats [19]
• Modulates both dopaminergic and serotonergic systems in a homeostatic manner — restoring balance rather than simply pushing neurotransmitter levels in one direction [19]
• Activates specific gene expression patterns in hippocampal tissue associated with neural recovery [19]

The gut-brain perspective: BPC-157 is native to human gastric juice. Its central nervous system effects appear to operate partly through visceral relay pathways and circumventricular organs — brain regions without a blood-brain barrier. This makes it one of the few peptides whose cognitive effects may not require direct brain penetration [19].

Limitations: No direct studies in age-related cognitive decline. Evidence is primarily from acute injury models rather than chronic aging. However, its safety profile in animal studies and early human trials (for inflammatory bowel disease and multiple sclerosis) is encouraging [19].

Pinealon

Pinealon (EDR, Glu-Asp-Arg) is a tripeptide derived from the neuroprotective drug Cortexin, studied primarily in Russian aging research.

Cognitive aging evidence:

• Oral administration improved memory, attention, cognitive function, and mental performance speed in elderly patients [20]
• In clinical trials involving 72 people with traumatic brain injury, Pinealon improved memory and cognitive performance. A separate trial reported improved working memory in 59.4% of subjects [20]
• The peptide crosses the blood-brain barrier and acts directly on neuronal DNA, activating genes involved in maintaining neuronal function and reducing apoptosis [20]
• In Alzheimer's disease models, Pinealon prevented dendritic spine loss in hippocampal neurons [20]
• Preclinical data shows a 40% reduction in markers of age-related neurodegeneration and a 35% decrease in oxidative stress markers (MDA levels) [20]

Anti-aging mechanism: Pinealon may support cellular lifespan through telomere-related pathways, including regulation of irisin production (associated with longer telomere length) and epigenetic modulation of 5-tryptophan hydroxylase expression in brain cortex cells [20].

Limitations: Most evidence comes from Russian research institutions. Pinealon is not FDA-approved, and large-scale, internationally validated clinical trials are needed.

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Peptide Comparison Table

Peptide	Primary Target	Memory Mechanism	Human Data	Evidence Strength
Semax	BDNF/TrkB system	Hippocampal neurotrophin upregulation	Yes (healthy volunteers)	Strong preclinical + limited clinical
Cerebrolysin	Neurotrophic factors	Multi-target neuropeptide mixture	Yes (RCTs in Alzheimer's)	Moderate clinical (meta-analysis)
Dihexa	HGF/c-Met pathway	Synaptogenesis promotion	No	Strong preclinical only
PE-22-28	TREK-1 channels	Rapid hippocampal neurogenesis	No	Preclinical only
Davunetide (NAP)	Microtubule stability	Tau prevention, neuroprotection	Yes (Phase 2/3 trials)	Moderate clinical (sex-dependent)
Humanin	Mitochondrial function	Anti-amyloid, synaptic support	Genetic association data	Strong preclinical + genetic
MOTS-c	AMPK pathway	Metabolic/energy optimization	Early clinical trials	Limited cognitive data
SS-31	Cardiolipin/mitochondria	Oxidative stress reduction, BDNF support	Heart failure trials	Strong preclinical, weak clinical
Selank	GABA/serotonin/dopamine	Stress reduction, neuroplasticity	Yes (anxiety trials)	Moderate clinical (indirect)
BPC-157	Gut-brain axis, dopamine	Homeostatic neurotransmitter modulation	Early IBD/MS trials	Strong preclinical
Pinealon	Neuronal gene expression	Anti-apoptotic, antioxidant	Yes (elderly patients)	Limited clinical

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What About Alzheimer's Disease?

Several peptides in this guide have been studied specifically in Alzheimer's disease models, but it's important to distinguish between age-related memory decline and Alzheimer's.

Normal age-related memory loss involves gradual hippocampal shrinkage, reduced BDNF, and declining synaptic plasticity — but the underlying neurons remain largely intact. Alzheimer's disease involves specific pathological processes: amyloid plaque accumulation, tau tangle formation, and progressive neuronal death.

Some peptides address both:

• Humanin was discovered specifically in the context of Alzheimer's neuroprotection and has anti-amyloid properties [15]
• Cerebrolysin has meta-analytic evidence in mild-to-moderate Alzheimer's [9]
• Davunetide stabilizes microtubules and prevents tau pathology [13]
• Dihexa showed promise in Alzheimer's-relevant animal models [11]

Others — like Semax, Selank, and SS-31 — target more general mechanisms (BDNF, neuroinflammation, oxidative stress) that are relevant to both normal aging and neurodegenerative disease.

For dedicated coverage of peptides in neurodegenerative conditions, see our guides on peptides for Alzheimer's disease and peptides for Parkinson's disease.

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Practical Considerations

Combining Approaches

Peptides targeting different mechanisms can theoretically complement each other. A neurotrophic peptide like Semax (boosting BDNF) paired with a mitochondrial peptide like SS-31 (reducing oxidative stress) would address two independent pathways contributing to age-related memory decline.

However, peptide combinations have rarely been studied together in rigorous trials. Any stacking approach should be discussed with a qualified physician. For general principles, see our peptide stacking guide.

Lifestyle Synergies

The same lifestyle factors that boost BDNF and improve mitochondrial function — aerobic exercise, quality sleep, caloric moderation, social engagement — also work synergistically with peptide mechanisms. A 2024 review in Frontiers in Aging Neuroscience found that even 35-minute sessions of physical exercise, cognitive training, or mindfulness practice increased BDNF levels in healthy older adults [3].

Peptides don't work in a vacuum. They work best alongside the fundamentals.

Regulatory Reality

None of the peptides in this guide are FDA-approved for memory enhancement or age-related cognitive decline. Cerebrolysin is approved in several European and Asian countries. Semax and Selank are approved in Russia. The rest are either in clinical trials or confined to preclinical research.

This means access is limited, quality control is inconsistent in unregulated markets, and individual use carries inherent risks. Working with a physician who understands both conventional cognitive medicine and peptide pharmacology is the safest approach.

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FAQ

Which peptide has the strongest evidence for memory improvement? Cerebrolysin has the most clinical trial data, with a meta-analysis showing statistically significant improvements in cognitive function and global clinical outcomes in Alzheimer's patients [9]. For non-diseased, age-related memory decline, Semax has the best combination of mechanistic evidence and human cognitive data.

Can peptides prevent age-related memory loss? No peptide has been proven to prevent memory decline in long-term, prospective human trials. The evidence supports their potential to support the biological pathways involved in memory — BDNF signaling, synaptic plasticity, mitochondrial function — but prevention claims require data we don't yet have.

Are mitochondrial peptides or neurotrophic peptides better for memory? They target different mechanisms. Neurotrophic peptides like Semax and PE-22-28 directly support neuron growth and synaptic connectivity. Mitochondrial peptides like Humanin and SS-31 address the energy deficit and oxidative stress that compromise neuronal function. The optimal approach may involve both.

How does Humanin differ from Semax for cognitive aging? Semax works primarily through BDNF upregulation and dopamine modulation — directly supporting synaptic plasticity and neurotransmitter function. Humanin works at the mitochondrial level, protecting neurons from energy failure, amyloid toxicity, and apoptosis. Semax has more direct human cognitive data; Humanin has stronger genetic association data linking its levels to real-world cognitive aging outcomes.

Is Dihexa safe for long-term use? The safety of long-term Dihexa use is unknown. No human clinical trials have been conducted. Its mechanism — activating the HGF/c-Met growth pathway — raises theoretical concerns about promoting uncontrolled cell growth. Until safety data from human trials is available, long-term use cannot be recommended.

Can these peptides help someone already diagnosed with Alzheimer's? Cerebrolysin has shown modest benefits in mild-to-moderate Alzheimer's in clinical trials. Davunetide showed sex-dependent benefits in a tauopathy. Humanin was specifically discovered in the context of Alzheimer's neuroprotection. However, none of these are standard-of-care treatments, and they should only be considered as part of a comprehensive treatment plan under medical supervision. See our guide on peptides for Alzheimer's disease for detailed coverage.

What lifestyle changes support the same pathways peptides target? Aerobic exercise is the single best non-pharmacological BDNF booster. Caloric restriction improves mitochondrial efficiency. Quality sleep supports memory consolidation and reduces neuroinflammation. Cognitive stimulation and social engagement support synaptic maintenance. These interventions work through the same pathways that peptides target and should be the foundation of any cognitive health strategy.

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The Bottom Line

Age-related memory decline is real, measurable, and driven by specific biological mechanisms — BDNF decline, synaptic plasticity changes, mitochondrial dysfunction, and neuroinflammation. Peptide research has identified compounds that target each of these mechanisms, some with human clinical data to support them.

Cerebrolysin has the most rigorous clinical evidence, with meta-analytic support in Alzheimer's disease. Semax has the strongest profile for BDNF-mediated cognitive support, backed by animal data and limited human studies. Humanin offers a uniquely compelling genetic story — its levels naturally predict cognitive aging in large human cohorts. And emerging peptides like PE-22-28 and Dihexa point toward a future where we might be able to stimulate new neuron and synapse formation directly.

But the field is young. Most evidence is preclinical. No peptide is a proven preventive for age-related memory loss, and none should replace evidence-based medical care. The most practical path is to build a foundation of exercise, sleep, nutrition, and social engagement — and to stay informed as the clinical trial data matures.

Your brain is not helpless against aging. The science of helping it is just getting started.

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References

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3. Bhatt, D., et al. (2024). "Neural ageing and synaptic plasticity: prioritizing brain health in healthy longevity." Frontiers in Aging Neuroscience, 16, 1428244. Frontiers

4. Grimm, A., & Eckert, A. (2017). "Brain aging and neurodegeneration: from a mitochondrial point of view." Journal of Neurochemistry, 143(4), 418-431. PubMed

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11. McCoy, A.T., et al. (2013). "Evaluation of metabolically stabilized angiotensin IV analogs as procognitive/antidementia agents." Journal of Pharmacology and Experimental Therapeutics, 344(1), 141-154. PubMed

12. Djillani, A., et al. (2017). "Shortened spadin analogs display better TREK-1 inhibition, in vivo stability and antidepressant activity." Frontiers in Pharmacology, 8, 643. PMC

13. Gozes, I., et al. (2024). "Davunetide sex-dependently boosts memory in prodromal Alzheimer's disease." Translational Psychiatry, 14, 118. Nature

14. Gozes, I., et al. (2023). "Unexpected gender differences in progressive supranuclear palsy reveal efficacy for davunetide in women." Translational Psychiatry, 13, 618. Nature

15. Yen, K., et al. (2018). "Humanin prevents age-related cognitive decline in mice and is associated with improved cognitive age in humans." Scientific Reports, 8, 14212. Nature

16. Kim, S.J., et al. (2023). "Mitochondria-derived peptide MOTS-c: effects and mechanisms related to stress, metabolism and aging." Journal of Translational Medicine, 21, 50. PMC

17. Zhao, W., et al. (2019). "Elamipretide (SS-31) improves mitochondrial dysfunction, synaptic and memory impairment induced by lipopolysaccharide in mice." Journal of Neuroinflammation, 16(1), 230. PMC

18. Kozlovskii, I.I., & Danchev, N.D. (2003). "The optimizing action of the synthetic peptide Selank on a conditioned active avoidance reflex in rats." Neuroscience and Behavioral Physiology, 33(6), 639-643. PubMed

19. Sikiric, P., et al. (2021). "Pentadecapeptide BPC 157 and the central nervous system." Neural Regeneration Research, 17(3), 482-487. PMC

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