The process known as "cognitive decline", popularly associated with the advance of age in humans, is not well understood. According to Bruce A. Yankner, a neurologist from Harvard, in an essay published in Nature for March 9, the connection between longevity and decreasing powers of thought ranked as a major medical issue during the 20th century. For philosophers, cognition is regarded as activity of thought and inference, to be distinguished from sensations, perceptions and feelings. Instead of explaining human activities as responses to stimuli, intellectual processes dependent upon inner mental states are recognised as spurs to action. These account for differences in individual responses to stimuli such as words, and to many grave social consequences, as manipulators of public opinion know well. The ability to age without loss of cognitive faculties is important for social cohesion, since it enables older individuals to assist in the care of children and allows young parents to carry out useful work in their community. The modern study of neurodegenerative diseases, writes Dr Yankner, was founded on the description in 1907 by Alois Alzheimer of a distinct type of dementia, and the observation of amyloid plaques in central nervous tissues. There are rare examples of early-onset dementia attributable to genetic mutations, but most dementias have their onset after the age of 65 years. Alzheimer's dementia is now recognised as a disease, and not as the inevitable consequence of ageing, where plaques do appear but not to the same extent as in true dementia. However, the two phenomena are probably related in some way. The majority of over-70s show some degree of cognitive impairment, particularly regarding short-term memory, and a clinical entity known as mild cognitive impairment is now recognised. "The continuum between normal ageing, mild cognitive impairment and Alzheimer's disease provides support for an old idea, namely that Alzheimer's disease may be an accelerated form of brain ageing . . ." The critical question is, if we live long enough, will we all become demented? Would therapeutic treatment of conditions such as Alzheimer's and Parkinson's diseases, characterised by abnormal accumulations of protein aggregates in central nervous tissue, retard the loss of cognitive ability in old age? Or will the anticipated further prolongation of the life-span be overshadowed inevitably by these disabilities?