Article

Revitalizing the Aged Brain

Department of Geriatric Psychiatry, Sheppard Pratt Health Systems, Memory Clinic, 6501 North Charles Street, Baltimore, MD 21204-6815, USA.
The Medical clinics of North America (Impact Factor: 2.8). 05/2011; 95(3):463-75, ix. DOI: 10.1016/j.mcna.2011.03.002
Source: PubMed

ABSTRACT Optimal cognitive and emotional function is vital to independence, productivity, and quality of life. Cognitive impairment without dementia may be seen in 16% to 33% of adults older than 65 years, and is associated with significant emotional distress. Cognitive and emotional well-being are inextricably linked. This article qualifies revitalizing the aged brain, discusses neuroplasticity, and suggests practical neuroplasticity-based strategies to improve the cognitive and emotional well-being of older adults.

2 Followers
 · 
103 Views
 · 
0 Downloads
  • [Show abstract] [Hide abstract]
    ABSTRACT: Interest surrounds the role of sex-hormones in regulating brain function outside of reproductive behaviour. Declining androgen production in aging males has been associated with cognitive impairment, depression and increased risk of developing Alzheimer's disease. Indication for testosterone replacement therapy is based on biochemically determined low circulating testosterone combined with manifest symptoms. However, which aspects of age-related cognitive decline are attributable to low circulating testosterone remain ambiguous. Studies examining cognition in aging men receiving testosterone replacement therapy have yielded equivocal results. The exact role of testosterone in maintaining cognitive function and the underlying neural mechanisms are largely unknown, though it would appear to be domain specific. Clarity in this area will provide clinical direction toward addressing an increasing healthcare burden of mental health decline coincident with increasing longevity. The premise that androgens contribute to maintaining aspects of mental health in aging men by preserving hippocampal neurogenesis will be used as a forum in this review to discuss current knowledge and the need for further studies to better define testosterone replacement strategies for aging male health.
    Neural Regeneration Research 10/2012; 7(28):2227-39. DOI:10.3969/j.issn.1673-5374.2012.028.009 · 0.23 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Alzheimer’s disease (AD) is a progressive neurodegenerative disorder. The human brain is extremely sensitive to hypoxia, ischemia, and glucose depletion. Impaired delivery of oxygen in obstructive sleep apnea (OSA) alters neuronal homeostasis, induces pathology, and triggers neuronal degeneration/death. This article systematically delineates the steps in the complex cascade leading to AD, focusing on pathology caused by chronic intermittent hypoxia, hypertension, brain hypoperfusion, glucose dysmetabolism, and endothelial dysfunction. Hypoxia/hypoxemia underpins several pathological processes including sympathetic activation, chemoreflex activity, neuroinflammation, oxidative stress, and a host of perturbations leading to neurodegeneration. The arterial blood flow reduction in OSA is profound, being about 76 % in obstructive hypopneas and 80 % in obstructive apneas; this leads to cerebral ischemia promoting neuronal apoptosis in neocortex and brainstem. OSA pathology also includes gray matter loss in the frontal, parietal, temporal, and occipital cortices, the thalamus, hippocampus, and key brainstem nuclei including the nucleus tractus solitarius. (18)F-FDG PET studies on OSA and AD patients, and animal models of AD, have shown reduced cerebral glucose metabolism in the above mentioned brain regions. Owing to the pathological impact of hypoxia, hypertension, hypoperfusion and impaired glucose metabolism, the adverse cardiovascular, neurocirculatory and metabolic consequences upregulate amyloid beta generation and tau phosphorylation, and lead to memory/cognitive impairment—culminating in AD. The framework encompassing these factors provides a pragmatic neuropathological approach to explain onset of Alzheimer’s dementia. The basic tenets of the current paradigm should influence the design of therapeutic strategies to ameliorate AD.
    Neurochemical Research 12/2012; 37(12). DOI:10.1007/s11064-012-0854-6 · 2.55 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: It is unclear whether physical activity in later life is beneficial for maintenance of cognitive function. We performed a systematic review examining the effects of exercise on cognitive function in older individuals, and present possible mechanisms whereby physical activity may improve cognition. Sources consisted of PubMed, Medline, CINAHL, the Cochrane Controlled Trials Register, and the University of Washington, School of Medicine Library Database, with a search conducted on August 15, 2012 for publications limited to the English language starting January 1, 2000. Randomized controlled trials including at least 30 participants and lasting at least 6 months, and all observational studies including a minimum of 100 participants for one year, were evaluated. All subjects included were at least 60 years of age. Twenty-seven studies met the inclusion criteria. Twenty-six studies reported a positive correlation between physical activity and maintenance or enhancement of cognitive function. Five studies reported a dose-response relationship between physical activity and cognition. One study showed a nonsignificant correlation. The preponderance of evidence suggests that physical activity is beneficial for cognitive function in the elderly. However, the majority of the evidence is of medium quality with a moderate risk of bias. Larger randomized controlled trials are needed to clarify the association between exercise and cognitive function and to determine which types of exercise have the greatest benefit on specific cognitive domains. Despite these caveats, the current evidence suggests that physical activity may help to improve cognitive function and, consequently, delay the progression of cognitive impairment in the elderly.
    Clinical Interventions in Aging 04/2014; 9:661-682. DOI:10.2147/CIA.S55520 · 1.82 Impact Factor
Show more