The present article examines several lines of converging evidence suggesting that
the slow and insidious brain changes that accumulate over the lifespan,
resulting in both natural cognitive aging and Alzheimer's disease (AD),
represent a metabolism reduction program. A number of such adaptive programs are
known to accompany aging and are thought to have decreased energy requirements
for ancestral hunter-gatherers in their 30s, 40s and 50s. Foraging ability in
modern hunter-gatherers declines rapidly, more than a decade before the average
terminal age of 55 years. Given this, the human brain would have been a
tremendous metabolic liability that must have been advantageously tempered by
the early cellular and molecular changes of AD which begin to accumulate in all
humans during early adulthood. Before the recent lengthening of life span,
individuals in the ancestral environment died well before this metabolism
reduction program resulted in clinical AD, thus there was never any selective
pressure to keep adaptive changes from progressing to a maladaptive extent.Aging foragers may not have needed the same cognitive capacities as their younger
counterparts because of the benefits of accumulated learning and life
experience. It is known that during both childhood and adulthood metabolic rate
in the brain decreases linearly with age. This trend is thought to reflect the
fact that children have more to learn. AD "pathology" may be a natural
continuation of this trend. It is characterized by decreasing cerebral
metabolism, selective elimination of synapses and reliance on accumulating
knowledge (especially implicit and procedural) over raw brain power (working
memory). Over decades of subsistence, the behaviors of aging foragers became
routinized, their motor movements automated and their expertise ingrained to a
point where they no longer necessitated the first-rate working memory they
possessed when younger and learning actively. Alzheimer changes selectively and
precisely mediate an adaptation to this major life-history transition.AD symptomatology shares close similarities with deprivation syndromes in other
animals including the starvation response. Both molecular and anatomical
features of AD imitate brain changes that have been conceptualized as adaptive
responses to low food availability in mammals and birds. Alzheimer's patients
are known to express low overall metabolic rates and are genetically inclined to
exhibit physiologically thrifty traits widely thought to allow mammals to
subsist under conditions of nutritional scarcity. Additionally, AD is examined
here in the contexts of anthropology, comparative neuroscience, evolutionary
medicine, expertise, gerontology, neural Darwinism, neuroecology and the thrifty
genotype.