age related cognitive decline
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2022 ◽  
Author(s):  
Pur Balance CBD Gummies

Pur Balance CBD Gummies - Age Related Cognitive Decline,Arthritis,Joint Pain And much, much more...


Author(s):  
K.A. Abbott ◽  
J.M. Posma ◽  
I. Garcia-Perez ◽  
C. Udeh-Momoh ◽  
S. Ahmadi-Abhari ◽  
...  

Increasing evidence proposes diet as a notable modifiable factor and viable target for the reduction of Alzheimer’s Disease risk and age-related cognitive decline. However, assessment of dietary exposures is challenged by dietary capture methods that are prone to misreporting and measurement errors. The utility of -omics technologies for the evaluation of dietary exposures has the potential to improve reliability and offer new insights to pre-disease indicators and preventive targets in cognitive aging and dementia. In this review, we present a focused overview of metabolomics as a validation tool and framework for investigating the immediate or cumulative effects of diet on cognitive health.


Nature Aging ◽  
2021 ◽  
Author(s):  
Omar Mossad ◽  
Elisa Nent ◽  
Sabrina Woltemate ◽  
Shani Folschweiller ◽  
Joerg M. Buescher ◽  
...  

2021 ◽  
Author(s):  
Michele M. Mulholland ◽  
Adrien Meguerditchian ◽  
William D. Hopkins

Age-related changes in cognition, brain morphology, and behavior are exhibited in several primate species. Baboons, like humans, naturally develop Alzheimer's disease-like pathology and cognitive declines with age and are an underutilized model for studies of aging. To determine age-related differences in gray matter covariation of 89 olive baboons (Papio anubis), we used source-based morphometry (SBM) to analyze data from magnetic resonance images. We hypothesized that we would find significant age effects in one or more SBM components, particularly those which include regions influenced by age in humans and other nonhuman primates (NHPs). A multivariate analysis of variance revealed that individual weighted gray matter covariation scores differed across the age classes. Elderly baboons contributed significantly less to gray matter covariation components including the brainstem, superior parietal cortex, thalamus, and pallidum compared to juveniles, and middle and superior frontal cortex compared to juveniles and young adults (p<0.05). Future studies should the relationship between the changes in gray matter covariation reported here and age-related cognitive decline.


2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. 198-199
Author(s):  
Amar Sahay

Abstract Memory imprecision is a hallmark of age-related cognitive decline and mild-cognitive impairment (MCI) and is characterized by increased memory interference and decreased stability of memory representations. Evidence from humans, non-human primates and rodents demonstrate reduced hippocampal neurogenesis, excitation-inhibition imbalance and inflexible hippocampal remapping during age-related cognitive decline and MCI. Developing strategies to reverse cognitive decline during aging and Mild Cognitive Impairment necessitates an understanding of molecular, cellular, circuit and network mechanisms that support memory functions of the hippocampus. Over the last decade we have built a multifaceted program grounded in basic neuroscience that is aimed at improving memory in aging and MCI. We have demonstrated how we can Rejuvenate the aged hippocampus by selectively increasing neurogenesis and how we can Re-engineer connectivity of aged inhibitory microcircuits to improve memory precision in aging. Ongoing efforts include strategies to Repairing neurogenic niche fitness by targeting intercellular communication in the aging hippocampus. In today’s talk I will present a fourth approach catalyzed by our discovery of the first transcriptional regulator of neural stem cell expansion in the adult hippocampus. We will present data in support of this claim and convey how this discovery may guide strategies to maintain cognitive reserve embodied in the pool of neural stem cells in the adult hippocampus.


2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. 553-553
Author(s):  
Walter Boot ◽  
Dawn Carr ◽  
Shayok Chakraborty ◽  
Zhe He ◽  
Mia Lustria ◽  
...  

Abstract The APPT project supports the early detection and treatment of age-related cognitive decline and dementia by 1) enhancing adherence to cognitive intervention and assessment protocols, 2) improving understanding of barriers to long-term adherence, and 3) developing algorithms for predicting and preventing adherence failures. Two randomized controlled trials will test an adaptive technology support system predicted to boost adherence to cognitive protocols over a period of six months within samples of older adults with and without cognitive impairment. These studies will provide insight into the benefits of adherence support, and individual difference factors that should shape the adherence protocol, informing the process of identifying individuals who would benefit from additional support and predicting and preventing extended adherence failures before they happen. These studies should improve early detection and treatment of cognitive decline, extend functional independence, and improve lives of those with cognitive impairment as well as the lives of their families.


2021 ◽  
Vol 17 (S2) ◽  
Author(s):  
Vibha Acharya ◽  
Kang‐Hsien Fan ◽  
Beth E Snitz ◽  
Mary Ganguli ◽  
Steve DeKosky ◽  
...  

2021 ◽  
Author(s):  
Tyler S Saunders ◽  
Amanda Heslegrave ◽  
Declan King ◽  
Sarah Harris ◽  
Craig W Ritchie ◽  
...  

INTRODUCTION: Plasma phospho-tau 181 (p-tau181) is a promising blood biomarker for Alzheimer's disease. However, its predictive validity for age-related cognitive decline without dementia remains unclear. Several forms of p-tau have been shown to contribute to synapse degeneration, but it is unknown whether p-tau181 is present in synapses. Here, we tested whether plasma p-tau181predicts cognitive decline and whether it is present in synapses in human brain. METHODS: General cognitive ability and plasma p-tau181 concentration were measured in 195 participants at ages 72 and 82. Levels of p-tau181 in total homogenate and synaptic fractions were compared with western blot (n=10-12 per group), and synaptic localisation was examined using array tomography. RESULTS: Elevated baseline plasma p-tau181 and increasing p-tau181 over time predicted steeper general cognitive decline. We observe p-tau181 in neurites, presynapses, and post-synapses in the brain. DISCUSSION: Baseline and subsequent change in plasma p-tau181 may represent rare biomarkers of differences in cognitive ageing across the 8th decade of life and may play a role in synaptic function in the brain.


Entropy ◽  
2021 ◽  
Vol 23 (12) ◽  
pp. 1574
Author(s):  
Diego Marcos-Martínez ◽  
Víctor Martínez-Cagigal ◽  
Eduardo Santamaría-Vázquez ◽  
Sergio Pérez-Velasco ◽  
Roberto Hornero

Neurofeedback training (NFT) has shown promising results in recent years as a tool to address the effects of age-related cognitive decline in the elderly. Since previous studies have linked reduced complexity of electroencephalography (EEG) signal to the process of cognitive decline, we propose the use of non-linear methods to characterise changes in EEG complexity induced by NFT. In this study, we analyse the pre- and post-training EEG from 11 elderly subjects who performed an NFT based on motor imagery (MI–NFT). Spectral changes were studied using relative power (RP) from classical frequency bands (delta, theta, alpha, and beta), whilst multiscale entropy (MSE) was applied to assess EEG-induced complexity changes. Furthermore, we analysed the subject’s scores from Luria tests performed before and after MI–NFT. We found that MI–NFT induced a power shift towards rapid frequencies, as well as an increase of EEG complexity in all channels, except for C3. These improvements were most evident in frontal channels. Moreover, results from cognitive tests showed significant enhancement in intellectual and memory functions. Therefore, our findings suggest the usefulness of MI–NFT to improve cognitive functions in the elderly and encourage future studies to use MSE as a metric to characterise EEG changes induced by MI–NFT.


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