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AimsCurrently available animal models incompletely capture the complex pathophysiology of Alzheimer's disease (AD), typically involving β‐amyloidosis, neurofibrillary tangle formation and loss of basal forebrain cholinergic projection neurones (CPN). While age‐dependent β‐amyloidosis and tau hyperphosphorylation are mimicked in triple‐transgenic mice (3xTg), experimental induction of CPN loss in these...
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