Abstract

“ALZHEIMER’S DISEASE IN YOUNG GENERATION”

Miss. Savai Puja Rameshwar*, Prof. Dr. Megha T. Salve, Mr. Chopade B. L.

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Abstract

Alzheimer’s disease (AD) is the most common form of dementia, accounting for 60–80% of cases and affecting nearly 50 million people worldwide, with projections rising to 139 million by 2050. First described in 1907 by Alois Alzheimer in his patient Auguste Deter, AD is a progressive neurodegenerative disorder marked by cognitive decline, memory loss, impaired language, and executive dysfunction, ultimately leading to loss of independence and mortality. Early-onset cases, though rare, have been documented, including the youngest reported diagnosis at 19 years of age in China. Pathophysiologically, AD is characterized by amyloid-β (Aβ) plaque accumulation, neurofibrillary tangles of hyperphosphorylated tau protein, hippocampal atrophy, oxidative stress, and neuroin flammation mediated by microglial activation. Clinical progression occurs in three stages: mild (memory lapses, poor judgment), moderate (disorientation, impaired recognition, hallucinations), and severe (loss of speech, recognition, and body function control). Major risk factors include advanced age, APOE ε4 genotype, female sex, and family history, while protective variants such as APOE ε2 and klotho genes reduce susceptibility. Epidemiologically, AD prevalence doubles every decade after age 65, with up to 50% of individuals affected by age 85. Current management combines pharmacological approaches—primarily cholinesterase inhibitors and memantine—with non-pharmacological interventions such as physical exercise, music, sleep regulation, and oxygen therapy to slow progression and improve quality of life. Despite advances, AD remains a major cause of disability, dependence, and mortality, highlighting the urgent need for preventive strategies, novel therapeutics, and comprehensive care models to address its rising global burden., the amyloid cascade, tau pathology, oxidative stress, and mitochondrial dysfunction are among the hypotheses. Clinically, AD develops in mild, moderate, and severe phases, culminating in total.

Keywords: Pathophysiologically, AD is characterized by amyloid-β (Aβ) plaque accumulation, neurofibrillary tangles of hyperphosphorylated tau protein, hippocampal atrophy, oxidative stress, and neuroin flammation mediated by microglial activation.