Below you’ll find the full webinar recording, followed by key takeaways and responses to additional audience questions.
Tuesday, February 10, 2026
Speaker: Robert Wright, MD, MPH, Ethel H. Wise Chair of the Department of Environmental Medicine, Co-Director of the Institute for Exposomic Research, Icahn School of Medicine at Mount Sinai
Moderator: Ellen Lautenberg, Advisory Board Chair, Institute for Exposomic Research
Key Takeaways from Dr. Wright’s talk
Brain health is a lifelong trajectory—risk begins many years before a diagnosis.
Alzheimer’s risk is shaped by exposures and health states across decades, including early life (even prenatal) influences and midlife risk factors.
Timing matters.
The same exposure can have very different impacts depending on when it happens, because developing systems (like the brain) are often more vulnerable. The Developmental Origins of Health and Disease (DOHaD) framework, first described by Dr. David Barker, shows how early-life conditions shape adult disease risk. Think of your child health as the foundation upon which your adult health is built.
Read Dr. Wright’s blog on the Fetal Origins of Adult Disease.
Small, practical choices can reduce harmful exposures and support brain health—starting now.
Recommendations include steps to improve indoor air quality, such as ensuring good ventilation or using a HEPA filter, reducing exposure to plastics and PFAS “forever chemicals,” getting your annual checkup, avoiding ultra-processed foods, exercising, getting enough sleep, and socializing – although it can be difficult, try to engage people daily in positive ways. This is clearly a healthy lifestyle.
We need better ways to “reconstruct the past” to understand factors that contribute to risk today.
Traditional studies of human health often start late in life—leaving earlier exposures and experiences as “black boxes.” Emerging tools (Electronic health records mining, AI and Large Language Models (LLMs), novel biomarkers like teeth and hair, geospatial mapping) can help fill in the missing chapters to help identify early life risk factors.
“Precision healthspan” can complement precision medicine.
While precision medicine focuses on treating disease, precision healthspan focuses on staying well, including staying well when you have a chronic illness by slowing or preventing its progression. By providing individuals with evidence-based actions they can take to reduce risk of disease, we can maximize quality of life across the lifespan.
Q&A
Are you looking at specific environmental toxicants that increase the risk of Alzheimer’s disease?
At the Mount Sinai Institute for Exposomic Research, we approach Alzheimer’s disease through a life-course and exposome framework. Rather than focusing on a single “smoking gun” toxin, we examine how multiple exposures (e.g., chemicals, diet, stress, social factors, built environment) with both positive and negative influences, interact over time to shape brain health trajectories.
Watch a video about how scientific findings can guide day-to-day protective steps that individuals, families, and communities can take to reduce harmful environmental exposures.
There is evidence linking certain environmental exposures—such as air pollution, pesticides, solvents, and metals—to cognitive impairments and neurodegenerative risk. For example, our research has found strong links between early life exposure to lead and other neurotoxic heavy metals and risk of ALS, childhood memory decay, autism, and childhood depression.
Do you think there will eventually be public health measures that can be taken to slow the increased incidence of Alzheimer’s?
Yes. We believe population-level interventions can meaningfully reduce risk or slow the progression of the disease. Interventions can be policy based or lifestyle choices—diet, exercise, socializing, not smoking, reducing alcohol, and limiting exposure to toxic chemicals.
Policies that reduce harmful exposures linked to cognitive decline—cleaner air standards, safer water infrastructure, healthier housing, workplace protections—are critical. At the same time, interventions in patient care that improve cardiometabolic health (diabetes prevention, blood pressure control, physical activity promotion) are strongly supported by evidence.
Effective science and health messaging is equally important. We see tremendous opportunity in engaging individuals who are already motivated to protect their health—especially those managing chronic conditions. Clear, actionable guidance can shift trajectories now, even as structural policies evolve.
You described studies in which Parkinson’s Disease risk could be predicted by analyzing handwriting many years prior to disease onset to detect tremors. How are researchers addressing the lack of handwritten documents amid the pervasive use of electronic platforms?
While still in early stages of development, AI is advancing this work. Brief writing, speech, or motor tasks could be incorporated into routine clinical visits and stored securely in electronic health records. Advances in digital health tools—including voice analysis and motor tracking—make it possible to monitor change over time without depending on archived documents. This aligns with emerging work in digital biomarkers and early detection in neurodegenerative disease.
Related reading: The Nun Study
How do you account for protective factors when reconstructing the history of risk factors?
Protective factors are central to our framework. Education, cognitive engagement, physical activity (even as simple as walking daily), high quality diet (lean meats, vegetables, avoidance of ultraprocessed foods), social connection, avoiding microplastics and forever chemicals (by using ceramic/stainless steel and reusable water bottle rather than plastic and non-stick cookware), and cardiometabolic stability (i.e. checking your glucose status with your physician to maintain normal levels) may all buffer risk. Research on “cognitive reserve” suggests that lifelong learning can help individuals maintain function.
Is the gut–brain axis primarily influencing Alzheimer’s disease, or are other neurodegenerative diseases similarly influenced?
Emerging evidence suggests microbiome-mediated inflammation and metabolic pathways may influence multiple neurodegenerative diseases, including Parkinson’s disease. However, this field is still evolving. We need more longitudinal and mechanistic research to understand how microbiome dynamics interact with environmental exposures across time.
Most medical professionals collect family history of illness. Has anyone analyzed these datasets for patterns?
Family history is widely used in clinical risk assessment but remains under-leveraged in life-course modeling. Keep in mind that families share environment as well as genetics so a family history can reflect the impact of environment. When combined with environmental and longitudinal health data, family history could illuminate gene–environment interactions and shared exposure patterns. Integration of genomic, environmental, and longitudinal data is an important frontier in precision healthspan research.