地域医療と健康教育

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Trends in Pathology, Pathophysiology and Treatment of Alzheimer's Dementia

Akeem G Owoola, Francesca Fernandez, Lyn R. Griffiths, Daniel A Broszczak

Objectives: The aim of this research was to review the literature on Alzheimer’s Dementia (AD) with a focus on impact of AD on patients with caregivers, underlying genetic and biochemical understanding of AD pathology, pathophysiology, and present therapeutic applications.

Design: In this review, a search of the literature up to December 2020 in Scopus, Web of Science, Medline, and PubMed were included, using search terms that include Dementia, Alzheimer’s dementia, impact of AD on patients, impact of AD on caregivers, genetic variance, AD pathogenicity, Amyloid beta peptide, hyperphosphorylated tau protein, amyloid beta plaque, age-related AD severity, AD microenvironment, microglia, synaptic loss, loss of neuron, loss of brain weight, long-term potentiation, synaptic plasticity, synapse, memory, N-methyl-D-aspartate receptors, calmodulin-dependent kinase II, Amino-3-hydroxyl-5-methyl-4-isoxazole-propionic acid receptors, protein kinase C, cAMP responsive element binding proteins 1 and 2, data reproducibility, Sequential window acquisition of all theoretical mass spectra mass spectrometry, AD experimental models, and methods of data generation. Research articles and case studies in English were picked out and questioned.

Results: AD is a significant cause of morbidity in the developed world. Without new treatments, the number of AD patients worldwide will rise to 100 million by the year 2050. With therapeutic approaches limited, there is currently no effective treatment of AD. Many failures and standstills in AD clinical trials are underpinned by our limited understanding of AD, inaccurate interpretation of pathological results, and strength of current models with their respective methods of generation.

Conclusion: Identification of new and promising strategies in AD therapy and prevention requires unravelling the complex interplay of numerous regulatory mechanisms at the biomolecular level.