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AD also extends beyond these pathological processes, and additional mechanisms such as synaptic dysfunction, microglial activity, astrocytic neuroinflammation play an important role as biomarkers of AD progression. In\u00a0vivo evaluation and quantification of these molecular processes are possible with positron emission tomography (PET) imaging. As disease\u2010modifying therapies are entering clinical use, biomarkers' importance for early diagnosis and longitudinal monitoring of the disease increases.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>A\u03b2 is the earliest signature of AD which can be measured with PET imaging, followed by tau\u2010PET positivity, which is highly specific and central for staging and longitudinal monitoring. FDG\u2010PET continues to serve as a gold standard for detecting neurodegeneration, challenged by emerging dual\u2010phase PET protocols for amyloid and tau imaging, which integrate perfusion as a measure of neurodegeneration and pathology information in a single session, enhancing diagnostic efficiency. Synaptic density imaging reveals early synaptic loss linked to cognitive performance and decline. Neuroinflammation tracers can visualize microglial and astrocytic activation, contributing to disease onset and progression. Novel PET tracers targeting alpha\u2010synuclein and TDP\u201043 show great promise for detecting co\u2010pathologies which can contribute to AD clinical heterogeneity.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>PET imaging has advanced the field by enabling visualization of AD\u2010related changes and providing measurable outcomes for clinical trials and disease\u2010modifying therapies. Imaging of related pathologies can further improve diagnostic accuracy and provide important insights into disease heterogeneity. 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