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Alzheimer's Association International Conference 2026

July 12-15, 2026 | London, United Kingdom, and Online

9954

Integrating Lifestyle, Clinical Features, And Neuroinflammation In Alzheimer’s Disease And Related Disorders

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Poster Presenter

Bruna Seixas-Lima

Authors

Bruna Seixas-Lima

Part of Topic

Integrating Lifestyle, Clinical Features, and Neuroinflammation in Alzheimer’s disease and Related Disorders

Bruna Seixas-Lima1, Pedro Rosa-Neto2, Cheryl Wellington3, Jennifer G. Cooper3, Durjoy Lahiri, MD, DM4, Tyler Roncero1, Dvir Dori1, Howard Chertkow1, and the CCNA study group.

1Baycrest Academy for Research and Education, Toronto, ON, Canada, 2McGill University, Montreal, ON, Canada, 3University of British Columbia, Vancouver, BC, Canada, 4Medicine, Queen's University, Kingston, ON, Canada

Key findings: Peripheral and neuroinflammation markers show distinct links to neurodegeneration and cognition; multiple mechanisms, rather than a single dominant process, underlie cognitive decline in aging and dementia.

Introduction:

•Inflammation is a key biological process implicated in neurodegeneration1,2.

•Peripheral inflammation (IL‑6) and neuroinflammation (GFAP) may influence cognition through overlapping or independent pathways2.

•It is unclear whether IL‑6 affects brain pathology via neuroinflammation or through parallel systemic mechanisms.

•We examined how lifestyle, clinical factors, IL‑6, and GFAP relate to neurodegeneration and cognition in group of aging adults with and without cognitive impairment and dementia.

Methods:

Section	Details
Participants	N = 591 adults from the COMPASS‑ND3 cohort Diagnostic groups: CU, SCI, MCI, V‑MCI, AD, Mixed
Peripheral Inflammation	IL‑6
Neuroinflammation	GFAP (astrocytic reactivity)
Neurodegeneration	pTau181, NfL, Aβ42/40, White matter volume
Clinical & Lifestyle Factors	BMI, comorbidities, sleep, nutrition
Cognition	MoCA
Analysis	Age adjusted structural equation model (SEM); General linear model (GLM) plots are presented to illustrate continuous relationships

Results:

Inflammation Predictors	Neurodegeneration	Cognition
IL‑6 ↑ with age, BMI, comorbidities	IL‑6 & GFAP → pTau181, NfL	MoCA associated with IL‑6, GFAP, pTau181, NfL, Aβ42/40
GFAP ↑ with age; ↓ with BMI, linked to more sleep	GFAP → Aβ42/40	Indirect effects from IL‑6 and GFAP to MoCA via pTau181 & NfL
IL‑6 did not predict GFAP → independent pathways	GFAP → Aβ42/40

Conclusion:

•Both IL‑6 and GFAP contribute to neurodegeneration and cognitive decline.

•IL‑6 and GFAP operate through partially independent pathways, not a single cascade.

•Neurodegeneration (pTau181, NfL) is a key mediator linking inflammation to cognition.

•Cognitive impairment reflected multiple interacting pathologies, reinforcing the view that multiple mechanisms, rather than a single dominant process, underlie cognitive decline in aging and dementia.

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