{'fraction_non_alphanumeric': 0.026068821689259645, 'fraction_numerical': 0.009384775808133473, 'mean_word_length': 5.315789473684211, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Synaptic vesicle protein SV2A imaging with [11C]UCB‐J as a novel biomarker of neurodegeneration in Alzheimer's disease

Synaptic loss is a known feature of symptomatic Alzheimer’s disease (AD). Conversely, abundance of synapses may confer resilience to cognitive decline in the presence of AD pathology. Currently, the extent and distribution of synapse loss during the asymptomatic stages of AD is unknown. Synaptic vesicle glycoprotein 2A (SV2A) is found on synaptic vesicles and recent developments in PET imaging provide the capability of assessing SV2A in vivo. [C‐11]UCB‐J is a high‐affinity ligand for SV2A currently being tested as a biomarker of neurodegeneration in AD. In this project, we are testing the extent to which loss of synaptic density tracks with cognitive decline, as well as determining the temporal course of synaptic loss in relation to development of regional amyloid and tau pathology, particularly in the asymptomatic phase of AD.