The article discusses the role of β-amyloid (Aβ) oligomers (AβOs) in the neurotoxicity and mitochondrial dysfunction that leads to neuronal death and Alzheimer's disease (AD). AβOs, which are soluble oligomeric forms of Aβ, are believed to be more harmful than Aβ fibrils and plaques, and are considered key factors in the development of AD. The article highlights the disruption of mitochondrial function by AβOs, which can lead to mitochondrial dysfunction, including changes in morphology, function, and dynamics. These disruptions can result in impaired ATP production, increased oxidative stress, and neuronal apoptosis. The article also explores the mechanisms by which AβOs cause mitochondrial damage, such as disrupting mitochondrial dynamics, altering the electron transport chain, and inducing oxidative stress. Additionally, the article discusses the potential of targeting mitochondrial dynamics and function as a therapeutic strategy to combat the neurotoxic effects of AβOs. The review emphasizes the importance of understanding the complex relationship between AβOs and mitochondrial damage to develop effective treatments for AD.The article discusses the role of β-amyloid (Aβ) oligomers (AβOs) in the neurotoxicity and mitochondrial dysfunction that leads to neuronal death and Alzheimer's disease (AD). AβOs, which are soluble oligomeric forms of Aβ, are believed to be more harmful than Aβ fibrils and plaques, and are considered key factors in the development of AD. The article highlights the disruption of mitochondrial function by AβOs, which can lead to mitochondrial dysfunction, including changes in morphology, function, and dynamics. These disruptions can result in impaired ATP production, increased oxidative stress, and neuronal apoptosis. The article also explores the mechanisms by which AβOs cause mitochondrial damage, such as disrupting mitochondrial dynamics, altering the electron transport chain, and inducing oxidative stress. Additionally, the article discusses the potential of targeting mitochondrial dynamics and function as a therapeutic strategy to combat the neurotoxic effects of AβOs. The review emphasizes the importance of understanding the complex relationship between AβOs and mitochondrial damage to develop effective treatments for AD.