Dear Colleagues,

Alzheimer's disease (AD) is a neurodegenerative disease primarily associated with brain aging. Despite decades of research and drug development, there remains no effective treatment for AD, largely due to the absence of a clear underlying mechanism. Recognized AD markers include the accumulation of extracellular beta-amyloid protein (Aβ) and the intracellular hyper-phosphorylated tau protein (p-Tau), which closely correlate with behavioral symptoms of progressive cognitive decline. Numerous factors contribute to the molecular and cellular pathways in the pathogenesis of AD, encompassing genetic mutations, neuroinflammation, impairment of the blood-brain barrier (BBB), mitochondrial dysfunction, oxidative stress, and imbalances in metal ions. Regardless of the different etiologies of neurodegenerative diseases, an imbalanced endogenous prooxidant/antioxidant equilibrium, alterations in the antioxidant defense system, and changes in vascular function and new vessel formation are generally considered critical factors that lead to brain aging and progressive neurodegeneration, ultimately culminating in the development of AD pathogenesis and clinical symptoms.

In this regard, the reduced release of the endogenous hormone melatonin from the pineal gland with advancing age increases their susceptibility to these diseases. Additionally, the pivotal role of angiogenesis in aging and Alzheimer’s disease is manifested through the intricate interplay between senescence, oxidative stress, and extracellular matrix components. While significant progress has been made in understanding the various aspects underlying this devastating neurodegenerative disorder, future AD studies need to look into the underlying molecular mechanisms implicated in the detrimental conditions predisposing to neurodegeneration in aging, including the diminished role of melatonin. This pursuit is important for the development of accurate strategies for the diagnosis and treatment of AD.

Prof. Rumiana Tzoneva
Guest Editor

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