Introduction: Alzheimer’s is a progressive neurodegenerative disease affecting over 10 million people annually. While the exact cause remains elusive, research indicates that the accumulation of beta-amyloid plaques plays a significant role in the disease's complexities. Recent studies suggest that disturbances in the axonal transport of mitochondria within nerve cells may be a reason for nervous disorder in this disease. Search Method: Extraction of data from at least 16 articles utilizing databases such as Science Direct, Google Scholar, Medline, and PubMed, focusing on keywords: axonal transport, neurodegenerative diseases, Alzheimer's, mitochondrial transport, and cognitive impairment. Results: Axonal transport relies on three main factors: motor proteins, microtubules, and cargo, and disruption in any of these components can lead to impaired axonal transport. In Alzheimer’s, mitochondrial distribution is disrupted, with healthy mitochondria less visible in axon ends and dendrites. As new mitochondria transport from the cell body to axon ends, and worn-out mitochondria return for digestion, disturbances in axonal transmission affect this vital process. Research in animals has shown a direct relationship between disruptions in the structure of kinesin and dynein (motor proteins) and incorrect mitochondrial distribution, alongside neuronal integrity issues and electrical message transmission disturbances. Conclusion: Understanding axonal transfer factors as early indicators of the disease and their influence on mitochondrial distribution in Alzheimer’s offers a promising avenue for treatment approaches. By targeting axonal transport mechanisms, interventions could potentially mitigate the progression of this debilitating neurodegenerative condition.