Alzheimer’s disease represents a paradox in which the brain’s intrinsic capacity for neuroplasticity fails to prevent progressive decline. Unlike stroke, where intact circuits can reorganize and restore function, AD is marked by diffuse degeneration and active molecular brakes that suppress recovery. This article reviews the dual barriers of myelin-associated inhibitors and chronic neuroinflammation, and further considers the philosophical implications of conditional plasticity. Therapeutic strategies must therefore aim both to release inhibitory signaling pathways and to support the structural substrate of cognition.
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Published on: Oct 2, 2025 Pages: 17-18
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DOI: 10.17352/aadc.000031
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