Neuroprotective Peptides and Their Role in Alzheimer’s

Human dopamine levels in the brain decline after age 45, especially in the striatum (a key subcortical structure in the brain that plays a crucial role in motor control, decision making, reward processing and habit formation). Whilst this decline is a natural aspect of biological aging, dopamine deficiency in this area of the brain can lead to symptoms such as motor dysfunction, impaired motivation and desire for “rewards” (pleasure), a loss of automatic habits and behaviours such as getting dressed or brushing teeth and cognitive dysfunction. All of these, plus other symptoms, can be linked with Alzheimer’s disease as well as other conditions such as Parkinson’s.
There is significant variability in the rate of neurological aging across individuals, often influenced by a combination of genetic, environmental, and lifestyle factors. While some people experience relatively preserved cognitive and motor function well into old age, others may show early signs of decline and dopamine deficiency.
Other factors like cardiovascular health, physical activity, diet, education, stress, and exposure to toxins can all play a role in how the brain ages. Additionally, certain genetic predispositions may increase the risk of neurodegenerative conditions like Alzheimer’s or Parkinson’s disease
The Catecholaminergic Engine in Humans
The “Catecholaminergic Engine” in humans is a conceptual term used by neuroscientist Dr. József Knoll to describe the functional role of catecholaminergic neurons. These are neurons that produce and release catecholamines like dopamine, noradrenaline (norepinephrine), and adrenaline (epinephrine) as the core drivers of mental and physical performance, alertness, motivation, and vitality.
Research and demonstrations in the 1980s of how the age-related decrease of dopamine content in the striatum affects cognitive function opened up findings to drugs that could delay this dopamine deficiency causing problems, as well as enhance catecholaminergic activity. Deprenyl and Selegiline were both involved in clinical trials as to how these drugs could help patients suffering from dopamine deficiency and associated neurodegenerative diseases.
Deprenyl and Neurodegenerative Disease
Key findings:
- Deprenyl (Selegiline) slows progression of Parkinson’s and Alzheimer’s diseases.
- Widely used in 49 countries as a neuroprotective drug.
- Most clinical studies initially focused on its MAO-B inhibition; very low doses of Deprenyl increase dopamine release without altering MAO-B activity.
Sources:
- DATATOP study – https://pubmed.ncbi.nlm.nih.gov/1801542/
- NEJM study – https://www.nejm.org/doi/full/10.1056/NEJM199301213280305
- Selegiline in the treatment of Alzheimer’s disease – https://pubmed.ncbi.nlm.nih.gov/10354658/
- L-deprenyl in Alzheimer’s disease – https://pubmed.ncbi.nlm.nih.gov/3107514/
- Monoamine ozidase inhibitors: Promising therapeutic agents for Alzheimer’s disease – https://www.spandidos-publications.com/10.3892/mmr.2014.2040
Implications of taking Deprenyl (Selegiline) for Anti-Aging and Cognitive Health
Enhancing mesencephalic enhancer regulation through use of these drugs may:
- Improve quality of life in later years.
- Delay onset of age-related diseases.
- Improve learning and sexual performance with age.
Peptides and their role in boosting cognitive function
Pineal peptides have been shown to regulate the body’s neuroendocrine, immune and cardiovascular systems as well as improving melatonin levels and sleep patterns. The pineal gland (a small endocrine gland in the brain) has long been linked with cognitive health and brain function as it is responsible for the regulation of melatonin, normalising circadian rhythms in order to ensure good sleep and aiding in neuroprotection.
As we age, the pineal gland is prone to calcification which results in lowered melatonin production and a greater risk of Alzheimer’s and other neurodegenerative symptoms. By boosting and normalizing pineal gland function and melatonin production, there is the potential to slow cognitive decline, improve sleep quality and delay the onset and progress of neurodegenerative symptoms.
Epitalon® and Epithalamin®
Epitalon® and Epithalamin® are both derived from the pineal gland and work to regulate melatonin and support neuroendocrine balance, both of which have beneficial effects on cognition and neuroprotection. They differ in their origin and formulation.
| Property | Epitalon® & Epithalamin® |
| Primary Action | Both regulate the production of melatonin and promote healthy circadian rhythms. |
| Effect on Telomeres | Both have been shown in studies to stimulate telomerase activity, helping maintain telomere length. |
| Anti-Aging Effects | Both exhibit geroprotective effects — delaying aging markers, improving immune response, and possibly extending lifespan. |
| Mechanism of Action | Both influence gene expression, hormonal regulation, and cellular repair pathways, particularly in the neuroendocrine system. |
| Research Origin | Both were developed and studied extensively in Russia by Professor Vladimir Khavinson and the St. Petersburg Institute of Bioregulation and Gerontology. |
Epitalon® is a synthetic, defined molecule tetrapeptide made in a laboratory environment, whereas Epithalamin® is a natural pineal gland extract with a complex mixture of peptides and proteins extracted from animal (primarily porcine) pineal glands.
Pineal Bioregulator (Nature’s Marvels™)
This is a bovine pineal gland peptide supplement designed to “activate” pineal function and melatonin production by triggering specific gene repair and regenerative pathways. It is typically taken as a “course” – two capsules daily for about 10–30 days, repeated 1–2 times annually depending on health needs.
Peptide bioregulators may support gene expression tied to cell repair and regeneration, although direct human trials in Alzheimer’s are lacking at this moment in time. There have been several trials using ultrashort peptides on animals, both in in vitro and in vivo AD models.
Personalized peptide protocols for early intervention have also been explored with peptides used as diagnostic probes for detection and to control early stage disease.
Sources:
- Neuroepigenetic Mechanisms of Action of Ultrashort Peptides in Alzheimer’s Disease – https://www.mdpi.com/1422-0067/23/8/4259
- Peptide treatment could reverse cognitive decline in Alzheimer’s disease – https://www.medicalnewstoday.com/articles/peptide-treatment-could-reverse-cognitive-decline-alzheimers-disease
- Use of Peptides for the Management of Alzheimer’s Disease: Diagnosis and Inhibition – https://www.frontiersin.org/journals/aging-neuroscience/articles/10.3389/fnagi.2018.00021/full
Combining Peptides with Lifestyle Interventions for Alzheimer’s Prevention
Various studies have shown that the synergistic effects of peptides are boosted when combined with a healthy and varied diet, adequate and regular exercise and cognitive training.
Key points
- A Mediterranean-style or anti-inflammatory diet enhances synaptic plasticity and may improve the brain’s responsiveness to peptide therapy.
- Aerobic exercise increases levels of brain-derived neurotrophic factor (BDNF), insulin-like growth factor-1 (IGF-1), and vascular health, which may amplify the neurodegenerative effects of peptides.
- Cognitive stimulation and training preserve executive function and memory, potentially extending the efficacy window for early-stage peptide interventions
Sources
- Lifestyle Modifications and Nutritional Interventions in Aging-Associated Cognitive Decline and Alzheimer’s Disease – https://www.frontiersin.org/journals/aging-neuroscience/articles/10.3389/fnagi.2019.00369/full
- Neuro-Nutrition and Exercise Synergy: Exploring the Bioengineering of Cognitive Enhancement and Mental Health Optimization – https://www.mdpi.com/2306-5354/12/2/208
- Effects of preventive interventions on neuroimaging biomarkers in subjects at-risk to develop Alzheimer’s disease: A systematic review – https://www.frontiersin.org/journals/aging-neuroscience/articles/10.3389/fnagi.2022.1014559/full