Alzheimer’s disease (AD)
Alzheimer’s disease (AD) is an inexorable neurodegenerative condition characterized by the gradual degeneration of neurons, impairment of neuronal connectivity, and ultimately, neuronal demise1. Neurons, the fundamental units of the nervous system, play a critical role in facilitating various crucial brain functions such as communication, metabolism, and repair. These intricate neuronal networks form a structural and functional basis for complex brain operations. In the context of Alzheimer’s disease (AD), it is observed that the damage primarily presents itself in specific brain regions, namely the hippocampus and the entorhinal complex. These regions are of utmost importance in memory formation2. As the pathological progression of the disease occurs, the cerebral cortex, a crucial neural substrate implicated in the intricate processes of language, reasoning, and social behavior, is likewise affected, thereby precipitating a diverse array of cognitive and functional deficits. During the advanced stages of Alzheimer’s disease (AD), there is pervasive damage across various regions of the brain, accompanied by notable reductions in the volume of brain tissue.
The precise etiology of Alzheimer’s disease (AD) remains predominantly enigmatic; however, scholarly investigations have yielded certain insights regarding putative determinants that may contribute to its pathogenesis3. Genetic mutations play a substantial role in the manifestation of early onset Alzheimer’s disease (AD). Conversely, late-onset AD is characterized by a multifaceted interplay between genetic predisposition, environmental factors, and lifestyle choices. Various factors have been implicated in the progression of Alzheimer’s disease (AD), including brain aging and age-related alterations resulting in brain atrophy, inflammatory processes, vascular impairment, generation of free radicals, and dysfunction of cellular mitochondria.
The APOE gene, specifically the APOE ε4 allele, has been identified as a well-established genetic susceptibility factor for late-onset Alzheimer’s disease (AD), contributing to an increased risk of disease onset4. Nevertheless, it is imperative to acknowledge that the presence of this particular gene does not ensure the manifestation of Alzheimer’s disease (AD), as individuals lacking this gene can still be vulnerable to ailments.
Notably, individuals diagnosed with Down syndrome, characterized by the presence of an additional copy of chromosome 21, exhibit a significantly heightened susceptibility to the development of Alzheimer’s disease (AD)1,2. The genetic locus located on chromosome 21 harbors a gene responsible for the synthesis of amyloid proteins that have been identified as causative agents of the pathogenesis of Alzheimer’s disease (AD).
Significant advancements have been made in the comprehension of Alzheimer’s disease (AD)1–3,5; however, the intricate and multifaceted characteristics of this ailment continue to present persistent obstacles for both researchers and healthcare practitioners. Ongoing endeavors in scholarly investigation and timely identification hold paramount significance in the advancement of efficacious therapeutic modalities and interventions aimed at enhancing the quality of life of individuals afflicted with Alzheimer’s disease.