Structural changes[ edit ] Aging entails many physical, biological, chemical, and psychological changes. Therefore, it is logical to assume the brain is no exception to this phenomenon. CT scans have found that the cerebral ventricles expand as a function of age.
More recent MRI studies have reported age-related regional decreases in cerebral volume. The different functions of different tissues in the brain may be more or less susceptible to age-induced changes. Grey matter consists of cell bodies in the cortex and subcortical nuclei, whereas white matter consists of tightly packed myelinated axons connecting the neurons of the cerebral cortex to each other and with the periphery.
One proposed mechanism for the observed age-related plasticity deficits in animals is the result of age-induced alterations in calcium regulation. Due to the complexity of the brain, with all of its structures and functions, it is logical to assume that some areas would be more vulnerable to aging than others.
Two circuits worth mentioning here are the hippocampal and neocortical circuits. Evidence in support of this idea from animal work has also suggested that this cognitive deficit is due to functional and biochemical factors such as changes in enzymatic activity, chemical messengers, or gene expression in cortical circuits.
It is also worth noting that areas such as the cingulate gyrus , and occipital cortex surrounding the calcarine sulcus appear exempt from this decrease in grey matter density over time. Certain language functions such as word retrieval and production were found to be located to more anterior language cortices, and deteriorate as a function of age.
Neurofibrillary tangles are composed of paired helical filaments PHF. However, unlike tangles, plaques have not been found to be a consistent feature of normal aging. Oxidative stress Cognitive impairment has been attributed to oxidative stress, inflammatory reactions and changes in the cerebral microvasculature.
Oxidative stress is the most controllable risk factor and is the best understood. The online Merriam-Webster Medical Dictionary defines oxidative stress as, "physiological stress on the body that is caused by the cumulative damage done by free radicals inadequately neutralized by antioxidants and that is to be associated with aging.
Compared to other tissues in the body, the brain is deemed unusually sensitive to oxidative damage. In 'normal aging', the brain is undergoing oxidative stress in a multitude of ways. The main contributors include protein oxidation, lipid peroxidation and oxidative modifications in nuclear and mitochondrial DNA. As telomere length is partly inheritable,  there are individual differences in the age of onset of cognitive decline.
This DNA damage includes the oxidized nucleoside 8-hydroxydeoxyguanosine 8-OHdG , single- and double-strand breaks, DNA-protein crosslinks and malondialdehyde adducts reviewed in Bernstein et al.
Increasing DNA damage with age has been reported in the brains of the mouse, rat, gerbil, rabbit, dog, and human. Young 4-day-old rats have about 3, single-strand breaks and double-strand breaks per neuron, whereas in rats older than 2 years the level of damage increases to about 7, single-strand breaks and double-strand breaks per neuron.
This led to the identification of a set of genes whose expression was altered after age They concluded that DNA damage may reduce the expression of selectively vulnerable genes involved in learning, memory and neuronal survival, initiating a pattern of brain aging that starts early in life.
Chemical changes[ edit ] In addition to the structural changes that the brain incurs with age, the aging process also entails a broad range of biochemical changes. More specifically, neurons communicate with each other via specialized chemical messengers called neurotransmitters.
Several studies have identified a number of these neurotransmitters, as well as their receptors , that exhibit a marked alteration in different regions of the brain as part of the normal aging process. Dopamine[ edit ] An overwhelming number of studies have reported age-related changes in dopamine synthesis, binding sites , and number of receptors.
Studies using positron emission tomography PET in living human subjects have shown a significant age-related decline in dopamine synthesis,  notably in the striatum and extrastriatal regions excluding the midbrain. Significant age-related declines in dopamine receptors, D2 and D3 were detected in the anterior cingulate cortex , frontal cortex , lateral temporal cortex, hippocampus , medial temporal cortex, amygdala , medial thalamus , and lateral thalamus  One study also indicated a significant inverse correlation between dopamine binding in the occipital cortex and age.
Studies conducted using PET methods on humans, in vivo, show that levels of the 5-HT2 receptor in the caudate nucleus, putamen, and frontal cerebral cortex, decline with age. Deficits in orientation are one of the most common symptoms of brain disease, hence tests of orientation are included in almost all medical and neuropsychological evaluations. Results have been somewhat inconclusive. Some studies suggest that orientation does not decline over the lifespan.
In contrast, younger people with normal memory have virtually no orientation problems"  p. So although current research suggests that normal aging is not usually associated with significant declines in orientation, mild difficulties may be a part of normal aging and not necessarily a sign of pathology. Changes in attention[ edit ] Many older adults notice a decline in their attentional abilities.
If older adults have fewer attentional resources than younger adults, we would expect that when two tasks must be carried out at the same time, older adults' performance will decline more than that of younger adults.
However, a large review of studies on cognition and aging suggest that this hypothesis has not been wholly supported. Similarly, one might expect older adults to do poorly on tasks of sustained attention, which measure the ability to attend to and respond to stimuli for an extended period of time.
However, studies suggest that sustained attention shows no decline with age. Results suggest that sustained attention increases in early adulthood and then remains relatively stable, at least through the seventh decade of life.
It is worth noting that there are factors other than true attentional abilities that might relate to difficulty paying attention. For example, it is possible that sensory deficits impact older adults' attentional abilities.
In other words, impaired hearing or vision may make it more difficult for older adults to do well on tasks of visual and verbal attention. Memory and aging Many different types of memory have been identified in humans, such as declarative memory including episodic memory and semantic memory , working memory , spatial memory , and procedural memory. As in so many other science disciplines, the nature and nurture debate is an ongoing conflict in the field of cognitive neuroscience.
Research focused on discovering the genetic component in developing AD has also contributed greatly to the understanding the genetics behind normal or "non-pathological" aging. This modulation in gene expression may be due to oxidative DNA damage at promoter regions in the genome.