The leading cause of dementia in elderly people, it is a progressive, irreversible, and thus incurable, neurological disease characterised by premature senile dementia that affects brain functions, including short-term memory loss, inability to reason, as well as the deterioration of language and the ability to care for oneself. There is an irreversible loss of neurons in particular brain areas such as the hippocampus and the polymodal association areas. Also, there is degeneration of the middle and smaller cerebral blood vessels at a cellular level. By the end of the disease, most, if not all the cortical brain areas, as well as many sub-cortical nuclei, have two different types of lesions: amyloid plaques and neurofibrillary tangles. It is similar to senile dementia, with the exception that it usually starts in the 40s or 50s. An estimated 3% of people between the ages of 65 and 74 have Alzheimer’s, rising to about half those aged 85 and over. Worldwide, it estimated that the disease affects 15 million people. It was first described by the neurologist Alois Alzheimer (1864-1915) in 1906, and he published his observations the next year in his monumental tome Alzheimer’s disease. Associating Alzheimer’s name with the disease was due to the anti-Freudian psychiatrist Emil Kraeplin (1856-1926), who was responsible for the term ‘dementia praecox’ [or what was later changed to schizophrenia by Eugen Bleuler (1857-1940)] and its distinction from manic depression].
bend-but-don’t-break philosophy of proto- col adherenceSee Cell adhesion molecules (CAMs), Cholinergic neurotransmitter system, Down’s syndrome, Entorhinal cortex, Hippocampus, Human Connectome Project (HCP), Nerve Growth Factor (NGF), Prion (proteinaceous infectious particle), Protein-folding problem, Sensory memory, short-term memory (STM) and long-term memory (LTM), Surrogate endpoint