Biomarker Discovery.

Alzheimer’s Disease (AD) is a progressive neurodegenerative disease that results in the loss of memory, motor function, ability to think, and other basic functions required for day-to-day life. The causes of the disease are still being investigated, but scientists and researchers have mostly agreed on one of the major genetic contributions to the disease. The excess buildup of two proteins, Tau and β-amyloid, limits communication between nerve cells or neurons. The buildup of these proteins only increases with the progression of the disease. This paper will discuss the genetic causes of AD, the process behind the formation of neurofibrillary tangles and amyloid plaques, recent neuroimaging techniques that help diagnose the disease, current symptomatic treatments, and upcoming future treatments that may be able to slow the progression of the disease significantly. Patients with AD exhibit a substantial accumulation of amyloid-β (Aβ) plaques and neurofibrillary tangles (NFTs) within their brains, accompanied by a cascade of pathological processes such as neuroinflammation, synaptic dysfunction, mitochondrial and bio-energetic disturbances, as well as vascular abnormalities. Collectively these processes may ; https://doi.org/10.1038/s41392-024-01911-3 ultimately lead to the death of neurons.[3,4] AD can be categorized into two types: early-onset familial Alzheimer’s disease (FAD) and late-onset Alzheimer’s disease (LOAD). FAD is rare (approximately 5% of AD cases) with typical disease onset at 65 years or younger, usually caused by gene variants of amyloid pre cursor protein (APP), presenilin (PSEN1) and PSEN2. LOAD is more common (~ 95% of AD cases) with disease onset older than 65 years and is associated with a combination of genetic (such as apolipo-protein E ε4 allele), environmental, and lifestyle factors [5]. In addition to these pathological hall marks, multiple alterations converge in the pathogenesis of AD. Elevated levels of inflammatory markers in AD patients indicate that neuroinflammation plays a significant role in disease pathogenesis [6] additionally, mitochondrial defects have been implicated in the exhaustion of nerve cells [7]. The disease is further