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Related Experiment Video

Updated: May 28, 2026

Quantitative 3D In Silico Modeling (q3DISM) of Cerebral Amyloid-beta Phagocytosis in Rodent Models of Alzheimer's Disease

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Molecular Mechanisms Underlying Alzheimer's Disease Pathogenesis: Comprehensive Overview.

Filomena Lo Vecchio¹, Annamaria la Torre¹, Carolina Gravina¹

¹Laboratory of Gerontology and Geriatrics, Fondazione IRCCS Casa Sollievo Della Sofferenza, San Giovanni Rotondo, 71013 Foggia, Italy.

International Journal of Molecular Sciences

|May 27, 2026

Summary

Alzheimer's disease (AD) is a progressive neurodegenerative disorder causing dementia. This study explores the complex molecular pathways and interacting factors contributing to AD's neurodegeneration and progression.

Keywords:

Alzheimer’s disease autophagy mitochondrial dysfunction neurofibrillary tangles stress response β-amyloid

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Area of Science:

Neuroscience
Gerontology
Pathology

Background:

Alzheimer's disease (AD) is the leading cause of dementia in the elderly, characterized by neurodegeneration and cognitive decline.
Key pathological hallmarks include beta-amyloid plaques and neurofibrillary tangles, leading to neuronal death and synaptic loss.
While aging is a primary risk factor, sporadic AD involves genetic, inflammatory, infectious, and environmental factors.

Purpose of the Study:

To elucidate the primary molecular pathways implicated in Alzheimer's disease pathophysiology.
To investigate the intricate cross-interactions between these molecular mechanisms in driving neurodegeneration.
To provide a comprehensive overview of AD pathogenesis for enhanced understanding and potential therapeutic targets.

Main Methods:

Literature review and synthesis of current research on Alzheimer's disease molecular mechanisms.
Analysis of studies detailing the roles of beta-amyloid, tau pathology, inflammation, and genetic factors.
Examination of the interplay between various risk factors including aging, lifestyle, and environmental exposures.

Main Results:

Identified key molecular pathways including amyloid cascade, tau hyperphosphorylation, neuroinflammation, and synaptic dysfunction.
Highlighted the significant contribution of aging as a non-modifiable risk factor for sporadic AD.
Demonstrated complex interactions between genetic predisposition, systemic inflammation, chronic diseases, infections, TBI, lifestyle, and environmental exposures in AD onset and progression.

Conclusions:

Alzheimer's disease pathogenesis is multifactorial, involving a complex interplay of molecular pathways.
Understanding these interactions is crucial for developing effective therapeutic strategies against neurodegeneration.
Further research into these pathways may reveal novel targets for preventing or treating Alzheimer's disease.