The slide titled "Microplastics and Neurodegenerative Risk" presents an evidence-based review. It explores emerging links between microplastics and neurodegenerative diseases such as Alzheimer's, Parkinson's, and ALS.

Microplastics and Neurodegenerative Risk

Evidence-Based Review of Emerging Links to Alzheimer's, Parkinson's, and ALS

Microplastics are defined as plastic particles smaller than 5 mm, categorized into primary ones from microbeads and synthetic fibers, and secondary ones from the degradation of larger macroplastics. Key sources include cosmetics, textiles, tire wear, and wastewater.

Definition and Sources of Microplastics

• Microplastics: plastic particles <5 mm in size
• Primary microplastics: microbeads, synthetic fibers
• Secondary microplastics: degradation of macroplastics
• Key sources: cosmetics, textiles, tire wear, wastewater

Human exposure routes to microplastics include ingestion through contaminated food and water like seafood, salt, and bottled water; inhalation of airborne particles in urban and industrial air; and limited dermal contact absorption. Daily intake involves thousands of particles per person.

Human Exposure Routes

• Ingestion: contaminated food/water (seafood, salt, bottled water)
• Inhalation: airborne particles in urban/industrial air
• Dermal contact: limited absorption
• Daily intake: thousands of particles per person

This slide introduces Section 04, titled "Evidence of Crossing Biological Barriers." It highlights translocation across key barriers, including the gut, lung, and blood-brain barriers.

Evidence of Crossing Biological Barriers

04

Evidence of Crossing Biological Barriers

Translocation Across Gut, Lung, and Blood-Brain Barriers

Microplastics translocate from the gut to lungs and brain via the bloodstream, lymphatics, and interconnected gut-lung-brain axis, with studies confirming their presence in rodent lung and brain tissue after ingestion (Duke et al., 2021; Jin et al., 2022). They penetrate the blood-brain barrier through endocytosis and transcytosis, detected in zebrafish and mouse brains post-exposure, especially polystyrene MPs ≤5μm (Prüst et al., 2020; Lee et al., 2023).

Microplastics Crossing Barriers incl. BBB

Source: Scientific literature on MP translocation

Neurotoxicity mechanisms include oxidative stress from ROS overproduction and mitochondrial dysfunction. Additional pathways involve inflammation via microglial activation and cytokine release, as well as protein aggregation like amyloid-beta and alpha-synuclein.

Mechanisms of Neurotoxicity

• Oxidative stress: ROS overproduction, mitochondrial dysfunction
• Inflammation: Microglial activation, pro-inflammatory cytokine release
• Protein aggregation: Amyloid-beta accumulation, alpha-synuclein disruption

Source: Microplastic exposure disrupts neuronal homeostasis via multiple pathways.

The slide presents study findings on microplastics (MPs) in Alzheimer's (AD), Parkinson's (PD), and ALS, linking epidemiological evidence like serum MPs to cognitive decline in AD, airborne MPs in PD, and water MPs in ALS. Animal studies show brain MPs contributing to Aβ plaques in AD, dopamine neuron loss in PD, and motor neuron pathology in ALS.

Study Findings: Alzheimer's, Parkinson's, ALS

Source: Epidemiological and Animal Studies

The slide highlights key limitations like few human studies and dosimetry gaps, alongside public health implications urging policies for microplastic reduction. It outlines future directions including longitudinal cohorts, nanoMP effects, and intervention strategies, closing with a call to act now on brain health through research funding and policy changes.

Limitations, Implications, Future Directions

**Limitations

• Few human studies
• Dosimetry gaps

Public Health Implications

• Policies for microplastic reduction

Future Directions

• Longitudinal cohorts
• NanoMP effects
• Intervention strategies

Closing: Act now to safeguard brain health. Call to Action: Advocate for research funding and policy changes today.**