Even limited hearing loss might be associated with cognitive decline. If true, early intervention with hearing aids might help people have better cognitive performance.
Michael Johns III, MD, online editor for JAMA Otolaryngology, speaks with Justin Golub, MD, MS, assistant professor of otolaryngology at Columbia University, whose research has shown that very mild hearing loss can be associated with cognitive disability.
Can you imagine if each word had its own colour, or you could ‘see’ different types of music?
Synesthetes can experience the ordinary world in some pretty extraordinary ways. In this video Jamie Ward explains the variety of different ways in synesthesia can manifest itself, and what is happening in the brains of those who experience it.
Jamie Ward is Professor of Cognitive Neuroscience at the University of Sussex. He has written books a number of books about neuroscience and synesthesia.
Synesthesia is a perceptual phenomenon in which stimulation of one sensory or cognitive pathway leads to involuntary experiences in a second sensory or cognitive pathway. People who report a lifelong history of such experiences are known as synesthetes. Awareness of synesthetic perceptions varies from person to person.[7] In one common form of synesthesia, known as grapheme–color synesthesia or color–graphemic synesthesia, letters or numbers are perceived as inherently colored. In spatial-sequence, or number form synesthesia, numbers, months of the year, or days of the week elicit precise locations in space (for example, 1980 may be “farther away” than 1990), or may appear as a three-dimensional map (clockwise or counterclockwise). Synesthetic associations can occur in any combination and any number of senses or cognitive pathways.
From Wikipedia
From a MedPage Today online article (April 2, 2020):
This relationship between higher glucose levels and poorer cognitive functioning extended beyond just CASI z-score, as well, Cukierman-Yaffe noted. Higher HbA1c levels were also tied to significantly poorer performance in other psychological tests, including the clock making test of executive functioning, test of discriminative ability, and for the test of verbal fluency.
Poorer glycemic control was tied to cognitive decline following a lacunar stroke in a prospective cohort study.
Among 942 individuals with type 2 diabetes who had a lacunar stroke, every 1% higher HbA1c was tied to a 0.06 drop in cognitive function at baseline measured by Cognitive Assessment Screening Instrument (CASI) z-score (95% CI -0.101 to -0.018), reported Tali Cukierman-Yaffe, MD, MSc, of Sheba Medical Center and the Sackler School of Medicine of Tel Aviv University in Israel.
From a JAMA Network Open online release (February 21, 2020):
Across the 6 studies of 8699 participants, mean age ranged between 70 and 74 years and mean gait speed ranged between 1.05 and 1.26 m/s. Incident dementia ranged from 5 to 21 per 1000 person-years. Compared with usual agers, participants with only memory decline had 2.2 to 4.6 times higher risk for developing dementia…
Those with only gait decline had 2.1 to 3.6 times higher risk. Those with dual decline had 5.2 to 11.7 times the risk…
Impaired mobility, such as slow gait, is associated with an increased risk of dementia, but the effect size of this association is generally modest.1–6 Identifying persons who experience both mobility decline and memory decline, a main symptom in the early stage of dementia, may have a greater prognostic value in assessing risk of dementia because the combination could identify a group in whom gait speed decline is at least in part caused by neurodegenerative pathologic conditions of the central nervous system rather than local musculoskeletal problems, such as sarcopenia or osteoarthritis.7–9 A recent study of 154 participants with mild cognitive impairment reported that those who declined in both cognition and gait speed had the highest risk of dementia.
From BMJ Journal “Gut” study (February 17, 2020):
We observed that increased adherence to the MedDiet modulates specific components of the gut microbiota that were associated with a reduction in risk of frailty, improved cognitive function and reduced inflammatory status.
Objective Ageing is accompanied by deterioration of multiple bodily functions and inflammation, which collectively contribute to frailty. We and others have shown that frailty co-varies with alterations in the gut microbiota in a manner accelerated by consumption of a restricted diversity diet. The Mediterranean diet (MedDiet) is associated with health. In the NU-AGE project, we investigated if a 1-year MedDiet intervention could alter the gut microbiota and reduce frailty.
Design We profiled the gut microbiota in 612 non-frail or pre-frail subjects across five European countries (UK, France, Netherlands, Italy and Poland) before and after the administration of a 12-month long MedDiet intervention tailored to elderly subjects (NU-AGE diet).
Results Adherence to the diet was associated with specific microbiome alterations. Taxa enriched by adherence to the diet were positively associated with several markers of lower frailty and improved cognitive function, and negatively associated with inflammatory markers including C-reactive protein and interleukin-17. Analysis of the inferred microbial metabolite profiles indicated that the diet-modulated microbiome change was associated with an increase in short/branch chained fatty acid production and lower production of secondary bile acids, p-cresols, ethanol and carbon dioxide. Microbiome ecosystem network analysis showed that the bacterial taxa that responded positively to the MedDiet intervention occupy keystone interaction positions, whereas frailty-associated taxa are peripheral in the networks.
Conclusion Collectively, our findings support the feasibility of improving the habitual diet to modulate the gut microbiota which in turn has the potential to promote healthier ageing.
From the Brain Plasticity Journal (Dec 26, 2019):
In conclusion, increased CRF (cardiorespiratory fitness) following this six-month intervention was associated with enhanced brain glucose metabolism in the PCC (posterior cingulate cortex), a region linked to AD, and cognition among late-middle-aged individuals at risk for AD. If these findings are supported by a larger-scale study, this would provide strong evidence that adults at risk for AD may enhance brain function and cognition by engaging in aerobic exercise training.
PCC glucose metabolism correlated positively with change in VO2peak (the highest value of VO2 attained upon an incremental or other high-intensity exercise test, designed to bring the sub- ject to the limit of tolerance)…Improvement in executive function correlated with increased VO2peak. Favorable CRF adaptation after 26 weeks of aerobic exercise training was associated with improvements in PCC glucose metabolism and executive function, important markers of AD.
Aerobic exercise has been associated with reduced burden of brain and cognitive changes related to Alzheimer’s disease (AD). However, it is unknown whether exercise training in asymptomatic individuals harboring risk for AD improves outcomes associated with AD. We investigated the effect of 26 weeks of supervised aerobic treadmill exercise training on brain glucose metabolism and cognition among 23 late-middle-aged adults from a cohort enriched with familial and genetic risk of AD.
Dr. Nilüfer Ertekin-Taner, neurogeneticist and behavioral neurologist, discusses characteristics of neurodegenerative diseases such as dementia, Alzheimer’s disease, and movement disorders. She also discusses her research on the complex genetics of Alzheimer’s disease, including identifying therapeutic targets and biomarkers. She highlights Mayo Clinic’s unique approach to patient care.
From the Journal of Sport and Health Science:
Therefore, promotion of adequate volumes and intensities of physical exercise (i.e., approximately 3 months of moderate-intensity aerobic exercise, with 2–3 sessions/week lasting not less than 30 min) represents an inexpensive and safe strategy for boosting BDNF (brain-derived neurotrophic factor) release that may preserve or restore cognitive function.
Taken together, the currently available data seemingly confirm the existence of a positive relationship between physical exercise and circulating BDNF levels, both in the short and long term, and also support the beneficial impact of training programs for amplifying the acute BDNF response.
From a University of Toronto Medicine article:
“There are two important takeaways from this paper. One is that poor sleep is associated with brain immune dysregulation or dysfunction,” says Lim, the corresponding author for the paper.
“The second part is that dysfunction appears to be further associated with impaired cognition.”
The study shows that in adults with fragmented sleep – where people were waking up repeatedly instead of sleeping soundly – there was an effect on microglia, and the cells showed signs of accelerated aging and other abnormalities.
The researchers were then able to identify that these changes in the microglia could be associated with worse cognition in older adults, both with and without Alzheimer’s disease.
To read full study: https://advances.sciencemag.org/content/5/12/eaax7331
To read more: https://medicine.utoronto.ca/news/research-suggests-fragmented-sleep-may-affect-brain-s-immune-cells-impair-cognition
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