Alzheimer's disease (AD) is the most common cause of dementia, which is characterized by progressive involutional changes in the brain. Establishing clear correlations between macroscopic manifestations of atrophy and underlying micromorphological pathological processes (formation of amyloid plaques and neurofibrillary tangles) is key to understanding the pathogenesis and developing diagnostic and treatment methods. Objective: To analyze current data on macroscopic and micromorphological changes in the brain in AD and their relationship with the clinical picture, with an emphasis on the possibilities of early diagnosis and treatment according to international recommendations. Materials and methods: A systematic review of the literature from 2018 to 2024 was conducted using PubMed, Google Scholar, and the Cochrane Library databases. Original studies, meta-analyses, and clinical guidelines on neuroimaging, pathomorphology, and biomarkers of AD met the inclusion criteria. Results: A close correlation was found between the sequential accumulation of pathological beta-amyloid (Aβ) and tau protein with specific macroscopic changes. Early atrophy of the medial temporal lobe, especially the entorhinal cortex and hippocampus, correlates with memory impairment and precedes significant cortical atrophy. According to PET imaging and cerebrospinal fluid biomarker studies, the pathological process begins 10-20 years before the onset of clinical symptoms. Current global guidelines (NIA-AA, 2018; IWG, 2021) shift the focus to the preclinical and prodromal stages, defining AD through biological markers. Conclusion: The integration of macroscopic neuroimaging data (MR morphometry) with the assessment of micromorphological changes using biomarkers (PET, cerebrospinal fluid) enables the diagnosis of AD at the earliest, potentially treatable stages. The advent of pathogenetic therapy aimed at clearing the brain of amyloid (aducanumab, lecanemab) makes early diagnosis clinically significant, opening up opportunities to slow the progression of the disease.

Alzheimer's disease, involutional changes, hippocampal atrophy

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