Autoimmune diseases (AIDs) emerge due to an irregular immune response towards self- and non-self-antigens. Inflammation commonly accompanies these conditions, with inflammatory factors and inflammasomes playing pivotal roles in their progression. Key concepts in molecular biology, inflammation, and molecular mimicry are crucial to understanding AID development. Exposure to foreign antigens can cause inflammation, potentially leading to AIDs through molecular mimicry triggered by cross-reactive epitopes. Molecular mimicry emerges as a key mechanism by which infectious or chemical agents trigger autoimmunity. In certain susceptible individuals, autoreactive T or B cells may be activated by a foreign antigen due to resemblances between foreign and self-peptides. Chronic inflammation, typically driven by abnormal immune responses, is strongly associated with AID pathogenesis. Inflammasomes, which are vital cytosolic multiprotein complexes assembled in response to infections and stress, are crucial to activating inflammatory processes in macrophages. Chronic inflammation, characterized by prolonged tissue injury and repair cycles, can significantly damage tissues, thereby increasing the risk of AIDs. Inhibiting inflammasomes, particularly in autoinflammatory disorders, has garnered significant interest, with pharmaceutical advancements targeting cytokines and inflammasomes showing promise in AID management.

Neurodegenerative diseases (NDs) encompass a group of chronic conditions, characterized by neuronal losses in large areas of the brain, leading to cognitive and behavioral impairments. Alzheimer’s Disease (AD), the most common form of dementia, is a progressive ND, characterized by the accumulation of amyloid β and tau protein, entails cognitive decline, neuroinflammation, mitochondrial dysfunction, and blood–brain barrier impairment, with oxidative stress playing a critical role in its pathogenesis. To date, the available pharmacotherapy has shown limited efficacy, and multitarget activity of plant-derived neuroprotective bioactive compounds is currently in focus. This review synthesizes experimental evidence regarding Ocimum species with neuroprotective potential in AD, particularly Ocimum sanctum and Ocimum basilicum. These plants are rich in bioactive compounds including polyphenols, flavonoids, essential oils, and triterpenoids that synergistically scavenge reactive oxygen/nitrogen species, upregulate endogenous antioxidant enzymes (SOD, CAT, and GPx), and reduce lipid peroxidation. Furthermore, these extracts have demonstrated the ability to decrease β-amyloid accumulation and tau protein levels, key pathological features of AD. Even though additional research is required to fully assess their potential as therapeutic agents for NDs, by diving into the specific mechanisms through which they improve neurodegenerative processes, important steps can be made towards this endpoint.