Orion Biomedica offers a comprehensive and individualized approach to the assessment and management of cognitive decline. This strategy is grounded in the latest scientific understanding of Alzheimer’s disease mechanisms and integrates conventional medical treatment with evidence-based nutritional and lifestyle interventions.
1. Identification of Key Risk Factors
A detailed evaluation of biochemical, genetic, and clinical parameters forms the foundation for a personalized treatment plan.
1.1 Laboratory Testing and Biomarkers
Inflammatory markers
- hs-CRP, IL-6, TNF-alpha
- Chronic inflammation may contribute to progressive neuronal damage.
Metabolic status
- Fasting glucose, insulin, HbA1c, HOMA-IR
- Assesses insulin resistance and glycemic regulation.
Homocysteine metabolism
- Elevated levels (>7 µmol/L) are linked to increased risk of cognitive decline.
- Assessment includes B6, folate (methylfolate), B12 (methylcobalamin), and betaine (TMG).
Hormonal and nutrient analysis
- Thyroid hormones (TSH, free T3, free T4, reverse T3)
- Sex hormones (estrogen, progesterone, testosterone, DHEA)
- Salivary cortisol, vitamin D, B12, B6, folate
- Magnesium, zinc, copper, and omega-3 fatty acids
Toxin and antioxidant status
- Heavy metals: mercury, lead, cadmium, arsenic
- Environmental chemicals: pesticides, plasticizers
- Glutathione levels as a marker of antioxidant capacity
Genetic factors
- APOE (especially APOE4), MTHFR, COMT, GSTM1/GSTT1 polymorphisms
1.2 Classification of Subtypes
To optimize treatment, Alzheimer’s disease is classified into three subtypes:
- Inflammatory (Type 1): Driven by chronic inflammation and immune activation
- Atrophic/Glycotoxic (Type 2): Marked by insulin resistance, hormone/nutrient deficiencies, and high homocysteine
- Toxic (Type 3): Associated with heavy metals, mold toxins, or synthetic chemical exposure
2. Key Mechanisms in Alzheimer’s Disease
- Amyloid beta and tau: Protein accumulation disrupts synapses and cytoskeletal integrity
- Mitochondrial dysfunction: Reduced ATP production, increased oxidative stress
- Chronic inflammation and insulin resistance: Amplify neuronal damage and protein misfolding
- Heavy metals and environmental toxins: Activate microglia and contribute to amyloid and tau pathology
- Selenium and selenoproteins: Support antioxidant systems and may reduce tau hyperphosphorylation
3. Treatment Strategies
3.1 Standard Medical Treatment
- Cholinesterase inhibitors (donepezil, rivastigmine, galantamine)
- Memantine
These medications may help sustain cognitive function temporarily.
3.2 Diet and Nutrition
- Ketogenic diet or intermittent fasting: Enhances ketone availability, improves metabolic flexibility
- Mediterranean diet: Rich in vegetables, fish, olive oil, and berries; supports anti-inflammatory pathways
Suggested targets
- Fasting insulin <6 mIU/L
- HbA1c <5.6%
3.3 Targeted Supplementation
- Omega-3 (EPA/DHA): 2–3 g/day for anti-inflammatory benefits
- Citicoline or Alpha-GPC: Supports acetylcholine synthesis
- Phosphatidylcholine: Enhances membrane integrity
- Coenzyme Q10: 100–300 mg/day; boosts mitochondrial function
- Curcumin, resveratrol: Antioxidant and neuroprotective properties
- Glutathione (liposomal or IV) and NAC: Support detoxification
- Baicalein: May reduce tau phosphorylation and amyloid burden
- Selenium (200 µg/day): Supports antioxidant defenses
- B vitamins + TMG: Maintain healthy homocysteine levels
- Alpha-lipoic acid: 300–600 mg/day; regenerates vitamins C and E
3.4 Mitochondrial Optimization
- Acetyl-L-carnitine: Enhances mitochondrial energy metabolism
- PQQ: Promotes mitochondrial biogenesis
3.5 Toxin Elimination
- Testing: Blood, urine, or hair samples for heavy metals
- Avoidance: Reduce exposure to mercury-containing fish, mycotoxins, and dental amalgam (with appropriate dental supervision)
- Support: Glutathione, NAC, and binding agents (e.g., activated charcoal, chlorella)
3.6 Gut Health Support
- Probiotics and prebiotics: Modulate systemic inflammation
- L-glutamine: Supports intestinal lining integrity
- Elimination diets: Applied in cases of suspected food intolerances
3.7 Physical Activity
- Aerobic and resistance training: Improve metabolic function and cerebral perfusion
- Balance exercises: Tai chi or yoga to enhance coordination and reduce fall risk
3.8 Stress and Sleep Management
- Mindfulness and meditation: Reduce chronic stress and protect hippocampal function
- Sleep optimization: Regular routines, reduced light exposure, and good air quality
3.9 Cognitive Rehabilitation
- Memory training: Often in collaboration with neuropsychologists or occupational therapists
- Social engagement: Preserves function and emotional well-being
3.10 Cardiovascular Risk Reduction
- Monitoring: Blood pressure, lipid levels, atrial fibrillation
- Goal: Improve cerebral blood flow and reduce vascular burden
4. Monitoring and Ongoing Adjustment
- Biomarkers: Monitored every 3–6 months (inflammation, insulin, homocysteine, metals)
- Cognitive assessments: Neuropsychological testing and functional status
- Protocol adjustments: Based on evolving clinical and laboratory data
- Multidisciplinary coordination: Including neurology, cardiology, endocrinology, dentistry, nutrition, and physiotherapy
- Palliative support: For advanced stages, prioritizing comfort and caregiver assistance
5. Conclusion
The approach at Orion Biomedica integrates multiple levels of intervention:
- Thorough laboratory diagnostics to identify modifiable risk factors
- Evidence-based medical treatment using approved pharmacologic agents
- Nutrition and lifestyle protocols tailored to the individual’s metabolic and genetic profile
- Precision supplementation targeting inflammation, mitochondrial health, and detoxification
- Regular follow-up with cognitive and biochemical monitoring
- Interdisciplinary collaboration to ensure holistic, patient-centered care
This proactive and personalized strategy aims to delay cognitive decline, maintain function, and support quality of life for as long as possible.
📞 For more information or to schedule a consultation, please contact Orion Biomedica.