The paper attempts to reconceptualize the pathological changes that accompany aging. It points out that many vital areas are spared by the senile plaques and tangles and that it is predominately the brain areas associated with learning new, higher-order concepts that are burdened with neuropathological load. These changes uncanilly follow another transition, seen in early adolescence, where rapid learning is slowed down because a large proportion of what a child needs to learn has already been learned. The demands on working memory seem to diminish throughout life and alzheimers may represent a pathological extension of an adaptive age-related decline in working memory function.
The original paper is entitled: "Alzheimer's Disease and Natural Cognitive Aging May Represent Metabolism Reduction Programs"
...Oh, added 12/12/11... The work was mentioned by an excellent article in Alzheimer's and Dementia entitled: "Some evolutionary perspectives on Alzheimer's disease pathogenesis and pathology." It was a very interesting article that should be read because of its insightful take on the history and function of neuritic plaques and neurofibrillary tangles. Here is some of what they had to say about the theory:
"Reser  discusses the intriguing possibility that preclinical or prodromal AD itself is an adaptation, a kind of “rescue program” that allows the body to conserve resources in food-scarce environments. Many other body systems downregulate in response to low caloric intake, shunting precious calories from the least crucial areas to the most vital ones, and because the brain is a bioenergetically high-cost organ, it might be expected to do the same. Reser suggests that the parts of the brain involved in attending to and encoding new information are expendable in a natural environment once an animal reaches the age where it has learned all the skills it needs to survive. In such an environment, the loss of the least crucial brain areas in exchange for precious calories is a utilitarian trade. In modern human society, however, those brain regions (the hippocampus and higher-order association cortices) are involved in domains that we now highly value, such as higher-level executive functions, personality, working memory, and episodic memory. Also, contemporary civilization, public health initiatives, and medical advances, especially in infectious disease, cardiovascular disease, and cancer, have extended the life span far beyond what we would assume to be that of Homo in the wild, who generally would have died of predation, starvation, injury, or infectious disease. Therefore, clinical AD, in Reser’s view, is “the unnatural progression of natural brain aging changes.” Circumstances notwithstanding, apoE influences the deposition, aggregation, activity, and neurotoxicity of Abeta, and APOE e4 correlates with increased Abeta load in AD patients relative to the other alleles . Next, we examine how Abeta and neurofibrillary tangles, the two signature pathologies of AD, fit into this integrated evolutionary picture and how evolutionarily informed research should approach them."