Mutated tau, amyloid and neuroinflammation in Alzheimer disease-A brief review

Area of Science:

• Neuroscience
• Pathology

Background:

• Alzheimer disease (AD) pathogenesis involves complex interactions.
• Key factors include mutated tau, amyloid plaques, and neuroinflammation.
• Microglia are central to the inflammatory response in AD.

Purpose of the Study:

• To review the interplay of mutated tau, amyloid, and neuroinflammatory factors in Alzheimer disease.
• To highlight the role of microglia and specific factors like CD4 and TNF alpha.
• To illustrate the co-localization and potential synergistic effects of these pathological elements.

Main Methods:

• Literature review focusing on molecular and cellular mechanisms in Alzheimer disease.
• Analysis of studies examining the co-occurrence of pathological hallmarks.
• Inclusion of a schematic representation of the proposed etiology.

Main Results:

• Mutated tau and amyloid aggregates often coexist in plaques.
• Neuroinflammatory factors, including CD4 and TNF alpha, are frequently found alongside these aggregates.
• Evidence suggests these factors interact and may contribute synergistically to disease progression.

Conclusions:

• Alzheimer disease etiology is likely multifactorial, driven by the interaction of genetic and inflammatory components.
• The co-localization of mutated tau, amyloid, and neuroinflammatory markers underscores their interconnected roles.
• Understanding these interactions is crucial for developing effective therapeutic strategies for Alzheimer disease.