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I first became aware of Galectin-3 listening to internist-cardiologist-epidemiologist Dr. Peter McCullough talk about it’s use in following heart damage post-Covid 19 vaccine. At the recent A4M Longevity Fest December 12-14, 2025 in Las Vegas I heard a very informative lecture on the
use of Galectin-3 as an assessment tool focused on neurologic disease and the use of anit-galectin-3 antibodies as a very promising treatment for Alzheimer’s disease and neurodegeneration. Here is a summary of the talk below. I personally am using Galectin-3 as a “high-end” C-reactive protein following not just heart disease and neurologic diseases but cancers and most other chronic diseases. Whatever chronic disease I am trying to help the patient with I have been monitoring levels of Galectin-3 and trying to get them below <17.8 ng/mL = low risk.

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Anti-Galectin-3 Antibody and How to Assess Individual Outcomes
James LaValle, RPh, CCN, MT & Sheldon Jordon, MD
(Longevity Fest 2025 12-12-25)

Galectin-3 is a central driver of chronic inflammation, neurodegeneration, and metabolic dysfunction, linking conditions such as Parkinson’s disease, Alzheimer’s disease, diabetes, heart failure, and fibrosis through shared inflammatory and immune pathways. James LaValle, RPh, CCN, MT explained how insulin resistance, gut-derived lipopolysaccharides (LPS), environmental toxins, and aging elevate Galectin-3, triggering microglial activation, oxidative stress, abnormal protein aggregation, and loss of neuronal function. Neurologist Sheldon Jordan, MD, then introduced TB-006, an investigational monoclonal antibody that blocks Galectin-3 and has shown early promise in improving cognition and motor symptoms in neurodegenerative patients. He emphasized that individual outcomes must be measured with sensitive tools—such as advanced MRI, proteomic biomarkers, and validated cognitive scales—to detect changes beyond placebo effects and natural variability. Galectin-3 inhibition was presented as a potentially transformative strategy in precision brain health and aging-related disease management.

Galectin-3 (Gal-3) is presented as a critical mediator linking:

• Neuroinflammation

• Metaflammation / Inflammaging

• Insulin resistance & metabolic syndrome

• Neurodegeneration (Parkinson’s, Alzheimer’s, post-TBI, etc.)

• Fibrosis & organ dysfunction (heart, kidney, liver, lung)

Galectin-3’s Role in Neuroinflammation

• Gal-3 is released by microglia in neuroinflammation

• Binds LPS and amplifies inflammatory signaling

• Promotes:

  • α-synuclein aggregation (Parkinson’s)

  • Tau phosphorylation (Alzheimer’s)

  • ROS generation

  • Fibrosis & tissue stiffening

• Persistently elevated Gal-3 creates self-propagating neuronal damage:

1. Neuron injury → release of α-synuclein & laminin fragments

2. Fragments → activate microglia

3. Microglia → produce more Gal-3

4. Gal-3 → amplifies inflammation + protein aggregation

Galectin-3 serum levels for chronic disease monitoring and risk reduction

• <17.8 ng/mL = low risk

• 17.8–22 ng/mL = moderate risk

• 22.2 ng/mL = high risk

• 25.9 ng/mL = rapid progression toward heart failure

Other markers frequently correlated with Gal-3:

• hs-CRP

• HbA1c / fasting glucose

• MMP-9

• Neutrophil/Lymphocyte ratio (NLR)

TB-006 is an investigational humanized monoclonal antibody developed by TrueBinding, Inc. that targets Galectin-3 (Gal-3), a protein involved in neuroinflammation and protein aggregation. It acts by inhibiting Gal-3, potentially reversing amyloid plaques and tau tangles to improve cognitive function in Alzheimer’s patients. TB-006 is available via FDA Expanded Access.

Proposed actions:

• Blocks Gal-3 binding

• Reduces α-synuclein aggregation

• Suppresses NLRP3 inflammasome

• Improves:

  • Synaptic function

  • Glymphatic clearance

  • Blood Brain Barrier integrity

  • Cognitive performance

1. Galectin-3 is a central amplifier of neuroinflammation

   • Strongly linked to Parkinson’s, Alzheimer’s, TBI, stroke, metabolic disease

2. Insulin resistance + LPS = Gal-3 activation

   • Supports “Type 3 diabetes” dementia model

3. Environmental toxicants are major contributors

   • Most Parkinson’s cases are non-genetic

4. TB-006 shows early promise

   • Objective improvements in cognition and motor function

   • Case videos showed dramatic Parkinson’s functional recovery

The Galectin-3 test measures a protein in the blood associated with inflammation and fibrosis (scarring) and is used “classically” to assess the risk, prognosis, and progression of heart failure. It helps clinicians identify patients with chronic heart failure at high risk for hospitalization or death, assisting in personalized treatment, disease management, and monitoring.

Traditional Reasons for the Galectin-3 Test:

• Heart Failure Prognosis: It is used alongside clinical evaluations to predict the severity and progression of chronic heart failure.

• Risk Assessment: Elevated levels (typically ng/mL) are associated with a higher hazard for mortality and re-hospitalization.

• Monitoring Disease Progression: Because Galectin-3 levels have low biological variability, regular testing (e.g., twice yearly) helps detect worsening heart failure, such as when levels increase by.

• Fibrosis Detection: Galectin-3 is a biomarker for cardiac, liver, and kidney fibrosis (tissue scarring).

• Preventive Strategy: Early detection of rising levels can lead to timely adjustments in treatment to prevent further cardiac damage.

Reducing Galectin-3 is an emerging area of immunology, metabolic health, and longevity research. There is evidence that certain dietary fibers, polyphenols, metabolic interventions, and gut/oral health strategies can help reduce Galectin-3 signaling or its downstream effects.

1. Natural Compounds
A. Modified Citrus Pectin (MCP)

• Most studied natural inhibitor of Galectin-3

• Binds Galectin-3 lectin domains and blocks its pro-inflammatory/fibrotic effects

• Used in cardiovascular fibrosis, kidney support, and cancer support research

• Doses vary in studies (often 5–15g/day, divided)

B. Green Tea Catechins (EGCG)

• EGCG inhibits Galectin-3 binding interactions in lab models

• Also reduces oxidative stress and inflammation

• Supports metabolic health

C. Curcumin (Turmeric Extract)

• Inhibits NF-κB, TLR-4, and inflammatory cascades linked to Galectin-3

• Shows anti-fibrotic actions in liver, kidney, and cardiovascular tissues

D. Resveratrol / Pterostilbene (dimethylated analog of resveratrol - more potent)

• Anti-fibrotic and anti-inflammatory signaling via AMPK activation

• Supports endothelial function and insulin sensitivity

E. Quercetin

• Inhibits mast cell activation and pro-fibrotic cytokines

• May blunt LPS-induced inflammatory pathways that upregulate Galectin-3

F. Berberine

• Improves insulin sensitivity and gut barrier function

• Reduces LPS translocation

• Helps reduce metabolic drivers of Galectin-3

G. Omega-3 Fatty Acids (EPA/DHA )

• Lower systemic inflammation

• Support neuronal and cardiovascular anti-fibrotic responses

2. Nutritional & Dietary Patterns

Certain patterns reduce the biological triggers that elevate Galectin-3:

A. Low-Glycemic, Insulin-Sensitizing Diet

Because insulin resistance is a major driver of Galectin-3:

• Emphasize vegetables, legumes, lean proteins, healthy fats

• Minimize refined sugars and ultra-processed carbs

B. Anti-Inflammatory Diet

Focus on:

• Olive oil, nuts/seeds, fish, berries, dark greens

• Spices (turmeric, ginger, garlic)

• Polyphenol-rich plants (tea, cacao, citrus)

C. High Fiber & Prebiotic Foods

Fiber reduces:

• Gut permeability

• Lipopolysaccharide (LPS) absorption

• Metainflammation

Sources:

• Beans/lentils, oats, chia, flax, root vegetables, leafy greens

D. Fermented Foods

Support microbial diversity:

• Kefir, yogurt, sauerkraut, kimchi, tempeh

3. Lifestyle Interventions That Lower Galectin-3 Drivers

A. Insulin Sensitivity & Metabolic Fitness

Exercise lowers insulin resistance, which strongly correlates with Galectin-3.

Most evidence supports:

• Zone 2 aerobic training (30–60 min, 4–5x/week) (Zone 2 training is a low-intensity, long-duration aerobic exercise performed at 60-70% of your maximum heart rate, often referred to as a "conversation pace").

• Strength training (2–3x/week)

• Intermittent fasting or time-restricted eating (if medically appropriate)

These improve:

• Mitochondrial function

• AMPK activation (AMPK ( AMP-activated protein kinase) activation acts as a master cellular energy sensor that restores energy balance by switching on catabolic pathways (fatty acid oxidation, glucose uptake, autophagy) and switching off anabolic pathways (cholesterol/protein synthesis). It is activated by low energy (high AMP/ADP-to-ATP ratio), exercise, calorie restriction, and compounds like metformin)

• Glucose utilization

• Neuroinflammation

B. Gut Health & Barrier Integrity

Because LPS upregulates Galectin-3, protecting the gut is key:

• Avoid frequent alcohol excess

• Minimize NSAID overuse (if applicable)

• Treat chronic GI issues (IBS, SIBO, IBD)

• Increase fiber + probiotics

C. Oral Health

Dental plaque contains LPS that drives Galectin-3.
Important steps:

• Brush & floss daily

• Dental cleanings 2x/year

• Treat gum disease promptly

D. Sleep & Stress

Poor sleep and chronic cortisol elevation amplify Galectin-3 pathways.
Helpful habits:

• 7–8 hours consistent sleep

• Morning light exposure

• Stress reduction (breathing, meditation, yoga, HRV training)

4. Environmental Factors to Reduce

Environmental toxins drive neuroinflammation and fibrosis.

Key contributors:

• Diesel/pollution

• Heavy metals (lead, mercury, cadmium)

• Mold/mycotoxins

• Pesticides & solvents

• Plastics & endocrine disruptors

Reducing exposure can indirectly lower Galectin-3 activation.

Inflamed

• Insulin resistant

• Exposed to toxins

• Under chronic immune stress
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