{'fraction_non_alphanumeric': 0.030612244897959183, 'fraction_numerical': 0.027696793002915453, 'mean_word_length': 5.481132075471698, '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}}
Pharmacological inhibition of c5a‐c5ar1 signaling decreases glial reactivity in a mouse model of Alzheimer’s disease

The complement system, a powerful effector mechanism of the immune system, can be activated by fAβ, leading to the generation of C5a. Upon binding to its microglial receptor (C5aR1), C5a‐C5aR1 signaling cascade contributes to neuroinflammation. Previous results have shown a beneficial effect of blocking C5a‐C5aR1 in Alzheimer’s disease (AD), either by a genetic ablation of C5aR1 or using a pharmacological approach. Here, we further examined the effect of a C5aR1 antagonist (PMX205) on the amyloid pathology and glial activation progression of a mouse model of AD.