Abstract

In the orchestrated objective reduction (Orch OR) theory of consciousness, information in the brain is proposed to be stored via quantum entanglement between fundamental units such as electron spins, electromagnetic fields, and the polarized molecules comprising neuronal microtubules. As an individual ages, environmental perturbations are hypothesized to progressively diminish the degree of quantum entanglement in these microtubules, thereby disrupting spin alignments and molecular polarizations. The resulting loss of quantum-coherent information is posited to manifest as memory loss and the cognitive decline characteristic of Alzheimer’s disease (AD). Importantly, this hypothesis also accounts for epidemiological observations that lifelong mental stimulation and social engagement may delay AD onset. Individuals with active thought processes and frequent neuronal signaling—such as those with rich social interactions or intellectual responsibilities—can sustain the energy levels required to maintain molecular polarization and entanglement, thereby preserving stored information. In contrast, prolonged inactivity or isolation may fail to provide sufficient stimulation to counteract entanglement decay. We present a theoretical framework and mathematical model, grounded in Orch OR, that links the loss of quantum entanglement in brain microtubules to the neuropathology of AD. The model demonstrates how entangled electron-spin states deteriorate over time and how elevated neuronal activity (modeled as electrical signals) can mitigate this deterioration. The results offer a quantum biological perspective on why active, socially-engaged lifestyles correlate with reduced AD risk, while advanced age and passive isolation correspond to increased vulnerability. This hypothesis article is structured as a scholarly exploration of the idea that Alzheimer’s disease may originate from the gradual loss of quantum coherence (entanglement) in the brain’s information processing microstructures, bridging quantum physics and neurobiology in the context of aging and dementia.