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The neuropathological features of Alzheimer's disease are the deposition of amyloid-β and the accumulation of tau protein
.
The pathology of neurofibrillary tau is closely related to key aspects of the neurodegenerative process
According to current understanding, neurons that initially undergo neurofibrillary disease will spread tau aggregates, which is similar to prions
.
Subsequently, as the tau seeds produced by the affected neurons enter healthy but fragile cells, where they change the physiological tau conformation, the tau pathology spreads in the brain along the neuronal pathway
More and more evidences show that aggregated tau, whether in free form or exosomal form, can be transferred from donor cells (neurons or glial cells) to recipient cells through various channels, including recipients Mediated (heparin sulfate proteoglycan, LDL receptor related protein 1) or non-receptor-mediated endocytosis/microprotein phagocytosis or transport via nanotubes (in vitro data)
.
Targeting tau is a potential treatment for AD
Recently, researchers reported the results of ADAMANT, a 24-month double-blind, parallel-arm, randomized phase 2 multicenter placebo-controlled trial in which AADvac1 is an active peptide vaccine designed to target AD Pathological tau protein (EudraCT 2015-000630-30)
.
During the trial, 11 doses of AADvac1 were administered to patients with mild AD dementia, each dose of 40 micrograms
.
The main goal is to evaluate the safety and tolerability of long-term AADvac1 treatment
immunity
The antibody response of AADvac1 treatment for more than 104 weeks shows that it has strong immunogenicity
.
.
The antibody response of AADvac1 treatment for more than 104 weeks shows that it has strong immunogenicity
AADvac1 is safe and well tolerated.
Original source:
Original source:Petr Novak et al.
et al.
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