Advances in Alzheimer's therapy: Exploring neuropathological mechanisms to revolutionize the future therapeutic landscape

Alzheimer's disease (AD) is still an excessively complicated neurological disorder that impacts millions of individuals globally. The ideal defensive feature of the central nervous system (CNS) is the intimate junction of endothelial cells, which functions as a biological barrier to safely control molecular transport throughout the brain. The blood-brain barrier (BBB) comprises tightly locked astrocyte cell junctions on CNS blood capillaries. This biological barrier shields the brain from hazardous toxins by preventing the entry of polar medications, cells, and ions. However, it is very challenging to provide any treatment to the brain for neurodegenerative illnesses like Alzheimer's. Different causative mechanisms, such as amyloid-β (Aβ) plaques, tubulin-associated unit (Tau) tangles, and neuroinflammation, cause neuronal dysfunction, leading to dementia and memory loss in the subject. Several treatments are approved for AD therapy, whereas most only help treat related symptoms. Disappointingly, current remedies have not been able to control the progression of AD due to associated side effects. Specific pathogenic mechanisms are involved in the initiation and development of this disease. Therefore, the expected survival of a patient with AD is limited and is approximately ten years. Hence, the pathogenic mechanism behind AD progression must be understood to better comprehend and improve the overall survival rate. This review highlighted the recent insights into AD pathogenesis, molecular mechanisms, advancements in theragnostic techniques, the existing updates of clinical trials, and emerging innovations for AD medicinal development. That has helped researchers develop other strategies to address the shortcomings of traditional medications.