Dyslipidemia may affect AD development through mechanisms involving ApoE4 levels, neuroinflammation, oxidative stress, cholesterol interactions with amyloid plaques and synaptic function, and vascular components. Increased cholesterol levels alter the blood-brain barrier’s permeability, potentially contributing to AD. ApoE, particularly its ε4 allele, is a significant genetic risk factor for AD. ApoE is involved in lipid transport and neural repair, with isoforms affecting AD pathology differently. ApoE4 is less effective in lipidation and promotes Aβ aggregation, reducing clearance and increasing deposition. This leads to neuroinflammation, tau hyperphosphorylation, and synaptic dysfunction. Cholesterol’s role in AD is linked to its influence on membrane properties, synaptic function, and Aβ production. High cholesterol levels can exacerbate Aβ generation and disrupt synaptic processes. Targeting these processes, along with managing dyslipidemia, offers potential pathways for mitigating AD progression.