Alzheimer’s disease (AD) is a prevalent neurodegenerative disorder characterized by memory loss, cognitive decline, and personality changes, largely resulting from the misfolding and aggregation of proteins such as amyloid-beta (Aβ) and tau. Similarly, prion diseases (PrD), though relatively rare, are highly lethal and transmissible, involving the misfolding of prion protein (PrP). Both conditions share common pathogenic mechanisms, including the aggregation of misfolded proteins that lead to neurodegeneration. This review compares the pathogenesis of AD and PrD, highlighting the similarities between the proteins involved and their impact on neuronal function. It explores current therapeutic strategies, particularly immunotherapy with monoclonal antibodies, which target pathogenic proteins like Aβ, tau, and PrP. While these treatments show promise in slowing disease progression and alleviating symptoms, challenges such as crossing the blood-brain barrier and managing toxicity remain significant. The findings suggest that insights from PrD may offer new avenues for AD treatment, underscoring the need for further research and clinical trials to develop more effective therapies for neurodegenerative diseases.
