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ALS: Disease or Neurotoxicity?

Exploring how pesticides and herbicides affect molecular processes associated with ALS.

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Herbicide · Glyphosate

Glyphosate results

01 · Glutamate reuptake / Glyphosate

Normal, ALS and glyphosate

Combined chart: normal approximately 2.30 nM, ALS 0.50 nM. Glyphosate inputs 0, 10, 20, 30, 40 and 50 mg correspond to approximately 2.30, 2.10, 1.90, 1.75, 1.65 and 1.55 nM. All glyphosate outputs remain above the ALS reference.
Biological Context

Uptake falls as glyphosate input rises. The source series declines from about 2.30 to 1.55 nM, a roughly one-third reduction relative to its zero-input result.

The series remains above the ALS reference. The 50 mg result is about 1.55 nM, compared with approximately 0.50 nM for ALS. This is a change in one model readout, not evidence that glyphosate produces ALS.

02 · Intracellular calcium / Glyphosate

Normal, ALS and glyphosate

Intracellular calcium: normal 100 nM; ALS 1475.8 nM. Glyphosate inputs 0 mg: 100 nM, 10 mg: 159.4 nM, 20 mg: 221 nM, 30 mg: 285.3 nM, 40 mg: 352.6 nM, 50 mg: 423.3 nM.
Biological Context

Calcium rises with glyphosate input. The output increases from 100 nM at 0 mg to 423.3 nM at 50 mg, or 4.23 times its starting value.

The series stays below the ALS reference. The normal and zero-input results both equal 100 nM. The separate ALS reference is 1,475.8 nM; every supplied glyphosate result remains below it.

Additional pesticide comparisons

Chlorpyrifos and cyfluthrin results

03 · CHOP / Chlorpyrifos

Normal, ALS and chlorpyrifos

CHOP: normal 5.6899999999999995E-4 nM; ALS 1.425654701E-3 nM. Chlorpyrifos inputs 0 mg: 5.6918103452236401E-4 nM, 10 mg: 3.2393762588654902E-3 nM, 20 mg: 5.96271714434335E-3 nM, 30 mg: 8.69888498934469E-3 nM, 40 mg: 1.14748497590387E-2 nM, 50 mg: 1.4290346781104499E-2 nM.
Biological Context

CHOP rises across the supplied series. At 50 mg, the output is about 25.1 times its zero-input value.

Reference comparison. The 10–50 mg outputs exceed the ALS reference numerically. Equivalent simulation settings have not been established by the slides.

04 · Adenyl cyclase / Cyfluthrin

Normal, ALS and cyfluthrin

Adenyl cyclase: normal 2.8954112126509302E-32 nM; ALS 1.4548294830586899E-32 nM. Cyfluthrin inputs 0 mg: 2.8954112126509302E-32 nM, 10 mg: 2.43497491333437E-32 nM, 20 mg: 2.17902468375728E-32 nM, 30 mg: 1.98381550630684E-32 nM, 40 mg: 1.8229539798567101E-32 nM, 50 mg: 1.6860588634485101E-32 nM.
Biological Context

Adenyl cyclase decreases with cyfluthrin input. The output falls about 41.8% between 0 mg and 50 mg.

The series stays above the ALS reference. The normal and zero-input results now match. At 50 mg, the output is approximately 1.686 × 10⁻³² nM, compared with 1.455 × 10⁻³² nM for the separate ALS reference.

Beyond the model

What published research tells us

Human observational evidence

Pesticide exposure and ALS

Su et al. studied 156 people with ALS and 128 controls. Reported occupational pesticide exposure was associated with higher ALS odds (OR 5.09; 95% CI 1.85–14.0).

The study also assessed persistent pollutants. It does not establish glyphosate as a cause of ALS.

Su et al., 2016 [2] →
Experimental evidence in rats

Glyphosate-based herbicide and glutamate

Cattani et al. reported disrupted glutamate handling, calcium-related effects and oxidative stress in immature rat hippocampus after exposure to Roundup®, a glyphosate-based formulation.

Formulation and animal-model findings cannot be directly equated with pure glyphosate exposure or human ALS.

Cattani et al., 2014 [3] →
Human observational evidence

Pesticides and Parkinson’s disease

Tanner et al. found associations between Parkinson’s disease and use of rotenone or paraquat, with odds ratios of 2.5 for each in a case-control study.

These agents relate to mitochondrial dysfunction and oxidative stress. The findings do not imply identical effects for all herbicides.

Tanner et al., 2011 [4] →
Golf courses and environmental exposure

What does the golf-course study actually show?

A 2025 study of 419 Parkinson’s disease cases and 5,113 controls found higher odds among people living within 1 mile of a golf course than among those living more than 6 miles away. [5]

Course maintenance can involve pesticide use. The authors examined proximity and water-service characteristics as exposure proxies; drift and groundwater were possible pathways.

Who was studied matters. This was a study of residents, not golfers. It examined Parkinson’s disease, not ALS, and did not establish which pesticide caused the association. The results do not quantify a golfer’s personal risk.

2.26×

Adjusted odds of Parkinson’s disease
Within 1 mile vs. more than 6 miles

95% confidence interval: 1.09–4.70
Krzyzanowski et al., 2025 [5]

An observational association, not an absolute risk or proof of causation.

Sources & supporting material

Model graphics: user-supplied PowerPoint. The linked studies provide external context and did not generate the model outputs above.

  1. Rothstein et al. (1996). Knockout of glutamate transporters reveals a major role for astroglial transport in excitotoxicity and clearance of glutamate. Neuron, 16, 675–686.
  2. Su et al. (2016). Association of Environmental Toxins With Amyotrophic Lateral Sclerosis. JAMA Neurology, 73, 803–811.
  3. Cattani et al. (2014). Mechanisms underlying the neurotoxicity induced by glyphosate-based herbicide in immature rat hippocampus: involvement of glutamate excitotoxicity. Toxicology, 320, 34–45.
  4. Tanner et al. (2011). Rotenone, paraquat, and Parkinson’s disease. Environmental Health Perspectives, 119, 866–872.
  5. Krzyzanowski et al. (2025). Proximity to Golf Courses and Risk of Parkinson Disease. JAMA Network Open, 8, e259198.

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