EDITORIAL The Complex and Multifactorial Nature of Alzheimer’s Disease

detailed the clinical, biographical, and neuropathological history of two patients admitted under his care for pre-senile dementia [2]. In these reports, Alzheimer described these patients as suffering from a “state of profound mental impairment with prominent agnostic, aphasic, and apractic disturbances, ” which he brilliantly attributed to small “miliary foci ” and/or dense “bundles of fibrils ” [1,2]. Even after a century of research, we continue to use the association between cognitive decline and proteinaceous deposits as classic hallmarks of Alzheimer’s disease. With the spectacular advancements in medicine and technology in recent decades, life expectancy has significantly increased, and diseases once deemed untreatable can now be prevented or even cured. Nevertheless, even with the progress that has been made in improving human health, this shift in demographics has been accompanied by the increased appearance of chronic diseases associated with ageing. Among such disorders, Alzheimer’s disease remains one of the most feared, as it is an irreversible, largely age-related neurodegenerative brain disorder that is responsible for the gradual and insidious failure of cognitive function. Ageing is one of the most well-established risk factors for Alzheimer’s disease [3]; this disorder has emerged as the predominant form of dementia in the elderly, affecting one person in ten over the age of 65, and 50 percent of individuals over the age of 85 [4,5]. Although the specific causes of idiopathic Alzheimer’s disease remain unknown, the vast majority of genetic and pathological observations made over that the past two decades suggests that an initial and critical accumulation of amyloid-beta (A) is