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According to the A-tau interaction hypothesis, A and tau pathology, which results in synaptic dysfunction, neuronal death, and cognitive impairment (96), is determined by the intrinsic interaction with A and tau (A42 enhances tau phosphorylation, truncation, and aggregation, while tau can increase A synthesis)

Some patients experience mild injection site reactions, transient changes in sleep patterns as circadian rhythms adjust, or minor digestive changes as metabolism optimizes

Mutations in the X-linked cyclin-dependent kinase-like 5 (CDKL5/STK9) gene are associated with severe neurodevelopmental retardation

Myeloid deletion of nuclear factor erythroid 2-related factor 2 increases atherosclerosis and liver injury