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.