Secondary prevention is aimed at people in the very early clinical stages of AD, including those with mild cognitive impairment (MCI) and those in the very early stages of AD, by assessing, treating reversible etiologies, and correcting all intervenable risk factors. MCI is a clinical state between normal aging and mild dementia when there is memory impairment and or mild other cognitive dysfunction, but the individual’s socio-occupational or daily living functioning is not impaired and cannot be explained by known medical or neuropsychiatric disorders.Patients with MCI do not include people with cognitive impairment due to significant depression, mania, mental retardation, or other psychiatric disorders. Studies have found that people with MCI progress further into dementia, and many people with MCI already have early pathological changes of AD. Of course, there are also a number of MCIs that do not progress to dementia, and the exact mechanism for this is not yet understood. MCI is a clinical state between normal aging and mild dementia, therefore, delaying the transition from MCI to AD is very beneficial for patients. Currently, there is no specific treatment for MCI, but there are some interventions that clinicians should consider, including the use of CIs, anti-inflammatory drugs, estrogens, statins, and various antioxidants, the promotion of healthy lifestyles such as an appropriate increase in physical exercise, the avoidance of mental or physical stimulation, and the reduction of stress, as well as the active control of vascular risk factors such as diabetes mellitus, hypertension, and hyperlipidemia. These interventions are important in the prevention and treatment of MCI and in stopping its further development into dementia. Future Strategies for Delaying the Disease With the progress of research in epidemiology, autopsy, biological markers, and animal models of AD, many hypotheses exist about its pathophysiology. There is a need to refine therapeutic strategies for AD so that patients at risk of developing the disease are prevented. A 5-year controlled clinical trial of ginkgo biloba and placebo was conducted to ensure safety and efficacy, and to expand the study population, samples carrying different risks of morbidity, such as cases with a family history of AD and/or carrying predisposing genes, were selected; however, the expansion of the sample would limit the applicability of the overall study results. In terms of age of onset, genetics, and different stages of the disease, it is likely that therapeutic agents that target subgroups of AD will work best. For example, amyloid inhibitors may be most effective in young patients with amyloidosis; however, statins are effective in AD patients with vascular lesions, aminoglucan mimetics (gag-mimetics) work early in the course of AD, and immunotherapies targeting amyloidosis are most effective in the treatment of mild to moderate dementia. We have grasped the natural history of AD, and clinical trials targeting different phases have been successful, with CIs and memantine being used to treat symptoms at all stages of AD with favorable results. With the progress of AD drug therapy, the management model of AD has been gradually improved, and the new strategy of delayed disease treatment will bring new hope for AD patients.