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There are two main branches of the human stress response. The autonomic nervous system acts rapidly and is often referred to as our fight or flight response. The slow-acting arm of the stress response refers to the hypothalamic-pituitary-adrenal (HPA) axis, which triggers a hormone cascade resulting in the release of various hormones including cortisol. Healthy functioning of the HPA axis is tightly regulated by negative feedback, the endogenous self-regulatory mechanism of the system that terminates cortisol production. Alterations in HPA axis functioning are characterized by both hypo- and hypersecretion of cortisol in response to psychological stress and are typically associated with negative physical health outcomes as well as clinical pathology. What remains poorly understood is how HPA activity changes with age and the pathways through which these changes occur. In addition to changes associated with the normative aging process, age-related changes in cortisol may also be driven by the cumulative effects of stress experienced across the life span (e.g., traumatic stress); stressors unique to later life (e.g., caring for an ailing loved one); or health problems. Although research examining how the HPA axis might change with age is inconsistent, there appears to be reasonable evidence to suggest that: (1) both stress-induced and diurnal cortisol output may increase with age, potentially beginning with changes in the cortisol awakening response, (2) variability in cortisol production increases with age, (3) diurnal (i.e., daily) cortisol rhythms are preserved in later life, and (4) age-related differences in cortisol may be more distinct in men than in women. However, it remains unknown whether these changes in older adults’ physiology reflect maladaptive functioning of the HPA axis or interact with other health concerns to negatively affect overall psychophysiological health. Further research is needed to disentangle the interplay between aging and HPA axis functioning to better understand what alterations are associated with the normative aging process, when they occur, and how they influence longevity.

Article

Age-related hearing loss affects over half of the elderly population, yet it remains poorly understood. Natural aging can cause the input to the brain from the cochlea to be progressively compromised in most individuals, but in many cases the cochlea has relatively normal sensitivity and yet people have an increasingly difficult time processing complex auditory stimuli. The two main deficits are in sound localization and temporal processing, which lead to poor speech perception. Animal models have shown that there are multiple changes in the brainstem, midbrain, and thalamic auditory areas as a function of age, giving rise to an alteration in the excitatory/inhibitory balance of these neurons. This alteration is manifest in the cerebral cortex as higher spontaneous and driven firing rates, as well as broader spatial and temporal tuning. These alterations in cortical responses could underlie the hearing and speech processing deficits that are common in the aged population.

Article

Richard L. Doty

Decreased ability to smell is common in older persons. Some demonstrable smell loss is present in more than 50% of those 65 to 80 years of age, with up to 10% having no smell at all (anosmia). Over the age of 80, 75% exhibit some loss with up to 20% being totally anosmic. The causes of these decrements appear multifactorial and likely include altered intranasal airflow patterns, cumulative damage to the olfactory receptor cells from viruses and other environmental insults, decrements in mucosal metabolizing enzymes, closure of the cribriform plate foramina through which olfactory receptor cells axons project to the brain, loss of selectivity of receptor cells to odorants, and altered neurotransmission, including that exacerbated in some age-related neurodegenerative diseases.

Article

Brian P. Kenealy and Ei Terasawa

Female reproduction is an interplay between the hypothalamus, pituitary, and ovaries. While the gonadotropin releasing hormone (GnRH) neuron in the hypothalamus regulates gonadal function through the pituitary, GnRH neuronal activity is also profoundly influenced by ovarian steroid hormones. GnRH is released from GnRH neurons in a pulsatile manner after integration of a diverse array of internal and external milieus. Since the discovery of the mammalian GnRH molecule, over a dozen GnRH forms have been identified in the animal kingdom, and large numbers of publications in various lab animal and human studies suggest that GnRH neurons are regulated by multiple neuromodulators in the brain, such as kisspeptin, neurokinin B, β-dynorphin, neuropeptide Y, GnIH, GABA, glutamate, and glial factors. A recent emerging concept is that steroids synthesized locally in the hypothalamus, namely, neuroestradiol and neuroprogesterone, also contribute to the regulation of GnRH neuronal activity, and hence female reproduction. Together with modulation by various inputs and ovarian steroid feedback, GnRH neurons are responsible for puberty, cyclic ovulation, and menopause.