<p>Cardiovascular diseases (CVDs) and cognitive impairment syndromes, encompassing Alzheimer’s disease (AD) and vascular cognitive impairment (VCI), exhibit a robust epidemiological association; however, the underlying pathophysiological mechanisms that mediate this relationship remain to be fully elucidated. Mitochondria, as the cellular organelles central to energy metabolism, orchestrate multiple homeostatic processes, including adenosine triphosphate (ATP) synthesis, redox regulation, and calcium homeostasis. An increasing body of preclinical and clinical evidence suggests that mitochondrial dysfunction, characterized by bioenergetic failure, heightened oxidative stress, dysregulated calcium handling, and impaired mitophagy, contributes to the etiopathogenesis of both CVDs and cognitive impairment. This narrative review comprehensively synthesizes current scientific knowledge regarding the role of mitochondrial dysfunction in major CVDs, such as hypertension, coronary artery disease, and heart failure, as well as neurodegenerative and vascular cognitive disorders, including AD and VCI. The molecular pathways by which mitochondrial derangements act as a unifying pathophysiological link between these conditions are explored in detail, with a particular focus on the oxidative stress–inflammation cascade, damage to the vascular–neural unit, and systemic metabolic reprogramming. In addition, a critical appraisal of emerging therapeutic modalities targeting mitochondrial function is provided, including mitochondria-targeted antioxidants, bioenergetic modulators, and agents that enhance mitochondrial quality control mechanisms. By integrating insights from basic science research with clinical observations, this review aims to advance the understanding of the comorbidity of CVDs and cognitive impairment and to identify potential therapeutic targets with cross-disease applicability.</p>