scholarly journals Bilingualism and Language Education to Improve the Cognitive Health of Older Persons

2021 ◽  
pp. 1-20
Author(s):  
Cécil J. W. Meulenberg
Keyword(s):  
Language Proficiency ◽  
Older Persons ◽  
Cognitive Reserve ◽  
Language Education ◽  
Positive Effects ◽  
Age Related ◽  
Age Related Cognitive Decline ◽  
Multiple Languages ◽  
The Brain

This article explores whether lifelong bilingualism can be associated with delayed age-related cognitive decline, with cognitive (or brain) reserve as the mechanism that compensates by positively increasing the functional capacity of the brain for older persons. A structural review of recent psychoneurolinguistic studies shows that older bilinguals display several years of delay in dementia symptoms as compared to monolinguals, as well as that positive effects exist in bilingual brain networks, also related to other neurodegenerative disorders. The field is clearly missing an established methodology, nevertheless, lifelong bilingualism can be considered to induce cognitive reserve. Drawing from these implications, we hypothesize that successful ageing could be facilitated by the active use of multiple languages, and in this light, we discuss language education for older persons, the role of Third Age Universities, the implementation of crucial aspects in such courses, and the proper assessment of the effectiveness of language proficiency and cognition.

COGNITIVE AGING AND COGNITIVE RESERVE: POINT OF CONTACT

2020 ◽  
pp. 256-264
Author(s):  
В. С. Мякотных ◽  
А. П. Сиденкова ◽  
Е. С. Остапчук ◽  
И. А. Кулакова ◽  
Н. А. Белых ◽  
...  
Keyword(s):  
Cognitive Aging ◽  
Cognitive Reserve ◽  
Cognitive Disorders ◽  
The Elderly ◽  
Educational Process ◽  
Special Role ◽  
Age Related ◽  
The Central Nervous System ◽  
The One

Высокий риск когнитивных расстройств у лиц пожилого и старческого возраста заставляет, с одной стороны, искать их причины, с другой - возможности профилактики. В связи с этим в последние годы получило распространение понятие когнитивного резерва, подразумевающего совокупность количественных параметров головного мозга и его способности сохранять высокую функциональную активность в процессе старения и на фоне связанной с возрастом патологии головного мозга. Представленный в статье материал на основе обзора научной литературы освещает два основных момента, касающихся возможности сохранения когнитивного резерва, - гендерный и образовательный факторы. Указывается на разные возможности женщин и мужчин, связанные со структурными и функциональными особенностями ЦНС у представителей разного пола, и на особую роль поддерживаемого в течение всей жизни образовательного процесса. Обозначена авторская позиция о необходимости разделения понятий образования и образованности, то есть уровня общей культуры и создания удобного инструмента для определения последнего. Это, в свою очередь, помогло бы в разработке модели когнитивного резерва, нацеленной на предотвращение трансформации физиологического когнитивного старения в патологическое. The high risk of cognitive disorders in the elderly and senile age makes, on the one hand, to look for their causes, on the other - the possibility of prevention. In this regard, in recent years, the concept of cognitive reserve has become widespread, implying a set of quantitative parameters of the brain and its ability to maintain high functional activity in the process of aging and against the background of age-related brain pathology. The material presented in the article on the basis of the review of scientific literature highlights two main points concerning the possibility of preserving the cognitive reserve-gender and educational factors. It is pointed to the different opportunities of women and men associated with the structural and functional characteristics of the Central nervous system in representatives of different sexes and the special role of the educational process supported throughout life. The author’s position on the need to separate the concepts of education and the level of General culture, and the creation of a convenient tool for determining the latter is indicated. This, in turn, would help in the development of a cognitive reserve model aimed at preventing the transformation of physiological cognitive aging into pathological aging.

Contribution of a Metal-Peroxide Adduct to Neurodegeneration Is Due to Its Oxidative Protease Activity

1999 ◽  
Vol 54 (12) ◽  
pp. 1107-1114 ◽  
Author(s):  
Yuzo Nishida ◽  
Satoshi Nishino
Keyword(s):  
Prion Disease ◽  
Protease Activity ◽  
Reaction Scheme ◽  
Theoretical Point ◽  
Metal Compounds ◽  
Age Related ◽  
The Moment ◽  
The Brain ◽  
Lateral Sclerosis

Many hypotheses have been developed to explain aging and age-related neurodegenerative disorders; one of the most compelling is the role of oxidative stress to induce changes in protease activity in brains of patients of Alzheimer’s disease and prion disease. At the moment however, there is no clear answer how protein degradation may be achieved in the brain. We have observed that several metal compounds can degrade proteins in the presence of hydrogen peroxide, and elucidated the reaction scheme based on the new theoretical point for the reactivity of a metal-peroxide adduct with η1-coordination mode. In this article we would like to point out the importance of a copper(II)-peroxide adduct to promote neurodegenerative diseases such as prion disease and amyotrophic lateral sclerosis through its oxidative protease function.

scholarly journals Evidence of the Role of Omega-3 Polyunsaturated Fatty Acids in Brain Glucose Metabolism

Nutrients ◽  
2020 ◽  
Vol 12 (5) ◽  
pp. 1382
Author(s):  
Fabien Pifferi ◽  
Stephen C. Cunnane ◽  
Philippe Guesnet
Keyword(s):  
Fatty Acids ◽  
Glucose Metabolism ◽  
Polyunsaturated Fatty Acids ◽  
Brain Function ◽  
High Energy ◽  
Brain Glucose ◽  
Brain Glucose Metabolism ◽  
Age Related ◽  
The Brain

In mammals, brain function, particularly neuronal activity, has high energy needs. When glucose is supplemented by alternative oxidative substrates under different physiological conditions, these fuels do not fully replace the functions fulfilled by glucose. Thus, it is of major importance that the brain is almost continuously supplied with glucose from the circulation. Numerous studies describe the decrease in brain glucose metabolism during healthy or pathological ageing, but little is known about the mechanisms that cause such impairment. Although it appears difficult to determine the exact role of brain glucose hypometabolism during healthy ageing or during age-related neurodegenerative diseases such as Alzheimer’s disease, uninterrupted glucose supply to the brain is still of major importance for proper brain function. Interestingly, a body of evidence suggests that dietary n-3 polyunsaturated fatty acids (PUFAs) might play significant roles in brain glucose regulation. Thus, the goal of the present review is to summarize this evidence and address the role of n-3 PUFAs in brain energy metabolism. Taken together, these data suggest that ensuring an adequate dietary supply of n-3 PUFAs could constitute an essential aspect of a promising strategy to promote optimal brain function during both healthy and pathological ageing.

scholarly journals Food for thought: The role of appetitive peptides in age-related cognitive decline

2013 ◽  
Vol 12 (3) ◽  
pp. 764-776 ◽  
Author(s):  
Jim R. Fadel ◽  
Corinne G. Jolivalt ◽  
Lawrence P. Reagan
Keyword(s):  
Cognitive Decline ◽  
Age Related ◽  
Age Related Cognitive Decline

scholarly journals CCL11 or Eotaxin-1: An Immune Marker for Ageing and Accelerated Ageing in Neuro-psychiatric Disorders

2020 ◽  
Author(s):  
Mariya Ivanovska ◽  
Zakee Abdi ◽  
Marianna Murdjeva ◽  
Danielle Macedo ◽  
Annabel Maes ◽  
...  
Keyword(s):  
Mood Disorders ◽  
Brain Aging ◽  
Accelerated Ageing ◽  
Neuroinflammatory Disease ◽  
Inflammatory Conditions ◽  
Treatment And Prevention ◽  
Age Related ◽  
Thought Disorders ◽  
Age Related Cognitive Decline ◽  
The Brain

Background: CCL11 (eotaxin) is a chemokine with an important role in allergic conditions. Recent evidence indicates that CCL11 plays a role in brain disorders as well. Aims: This paper reviews the associations between CCL11 and aging, neurodegenerative, neuroinflammatory and neuropsychiatric disorders.Methods: Electronic databases were searched for original articles examining CCL11 in neuropsychiatric disorders.Results: CCL11 is rapidly transported from the blood to the brain through the brain-blood barrier. Age-related increases in CCL11 are associated with cognitive impairments in executive functions, episodic and semantic memory and, therefore, this chemokine was described as an “endogenous cognition deteriorating chemokine” (ECDC) or “accelerated brain-aging chemokine” (ABAC). In schizophrenia, increased CCL11 is not only associated with impairments in cognitive functions, but also with key symptoms including formal thought disorders. Some patients with mood disorders and premenstrual syndrome show increased plasma CCL11 levels. In diseases of old age, CCL11 is associated with lowered neurogenesis and neurodegenerative processes and, as a consequence, increased CCL11 increases risk towards Alzheimer's Disease. Polymorphisms in the CCL11 gene are associated with stroke. Increased CCL11 also plays a role in neuroinflammatory disease including multiple sclerosis. In animal models, neutralization of CCL11 may protect against nigrostriatal neurodegeneration. Increased production of CCL11 may be attenuated by glucocorticoids, minocycline, resveratrol and anti-CCL11 antibodies.Conclusion: Increased CCL11 production during inflammatory conditions may play a role in human disease including age-related cognitive decline, schizophrenia, mood disorders and neurodegenerative disorders. Increased CCL11 production is a new drug target in the treatment and prevention of those disorders.

scholarly journals Impaired Mitophagy in Neurons and Glial Cells during Aging and Age-Related Disorders

2021 ◽  
Vol 22 (19) ◽  
pp. 10251
Author(s):  
Vladimir Sukhorukov ◽  
Dmitry Voronkov ◽  
Tatiana Baranich ◽  
Natalia Mudzhiri ◽  
Alina Magnaeva ◽  
...  
Keyword(s):  
Glial Cells ◽  
Brain Aging ◽  
Cellular Level ◽  
Aging Brain ◽  
The Past ◽  
Age Related ◽  
Accumulation Of Damage ◽  
Quantity Control ◽  
The Brain

Aging is associated with a decline in cognitive function, which can partly be explained by the accumulation of damage to the brain cells over time. Neurons and glia undergo morphological and ultrastructure changes during aging. Over the past several years, it has become evident that at the cellular level, various hallmarks of an aging brain are closely related to mitophagy. The importance of mitochondria quality and quantity control through mitophagy is highlighted by the contribution that defects in mitochondria–autophagy crosstalk make to aging and age-related diseases. In this review, we analyze some of the more recent findings regarding the study of brain aging and neurodegeneration in the context of mitophagy. We discuss the data on the dynamics of selective autophagy in neurons and glial cells during aging and in the course of neurodegeneration, focusing on three mechanisms of mitophagy: non-receptor-mediated mitophagy, receptor-mediated mitophagy, and transcellular mitophagy. We review the role of mitophagy in neuronal/glial homeostasis and in the molecular pathogenesis of neurodegenerative disorders, such as Parkinson’s disease, Alzheimer’s disease, and other disorders. Common mechanisms of aging and neurodegeneration that are related to different mitophagy pathways provide a number of promising targets for potential therapeutic agents.

scholarly journals Association between plasma phospho-tau181 and cognitive change from age 73 to 82: Lothian Birth Cohort 1936

2021 ◽  
Author(s):  
Tyler S Saunders ◽  
Amanda Heslegrave ◽  
Declan King ◽  
Sarah Harris ◽  
Craig W Ritchie ◽  
...  
Keyword(s):  
Cognitive Decline ◽  
Cognitive Change ◽  
Synaptic Function ◽  
Blood Biomarker ◽  
Array Tomography ◽  
Age Related ◽  
Lothian Birth Cohort ◽  
Synapse Degeneration ◽  
Age Related Cognitive Decline ◽  
The Brain

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.

scholarly journals ROLE OF INSULIN IN BRAIN: DELVE INTO THE MOLECULAR MECHANISMS

2021 ◽  
Author(s):  
Sofia Khanam
Keyword(s):  
Molecular Mechanisms ◽  
Insulin Signalling ◽  
Diabetic Patients ◽  
Functional Activities ◽  
Mitochondrial Alterations ◽  
Age Related ◽  
The Brain ◽  
And Oxidative Stress

We have learned over the last several decades that the brain is an important target for insulin action. In central nervous system (CNS) it mainly affects feeding behaviour and various aspects of memory and cognition. Insulin signalling in CNS has emerged as a novel field of research since decreases brain insulin levels and signalling were associated to impaired learning, memory and age-related neurodegenerative diseases. Alterations of these functional activities may contribute to the manifestation of several clinical entities, such as central insulin resistance, type 2 diabetes mellitus (T2DM) and Alzheimer’s disease (AD). A close alliance between T2DM and AD has been reported, to the extent that AD is twice more frequent in diabetic patients. There are links between T2DM and AD through mitochondrial alterations and oxidative stress, altered energy and glucose metabolism, cholesterol modifications, dysfunctional protein O-GlcNAcylation, formation of amyloid plaques, altered Aβ metabolism and tau hyperphosphorylation. Herewith, we aim to integrate the metabolic, neuromodulatory, and neuroprotective roles of insulin in two age-related pathologies: T2DM and AD, both in terms of intracellular signalling and potential therapeutic approach.

scholarly journals Role of age-related alterations of the cerebral venous circulation in the pathogenesis of vascular cognitive impairment

2019 ◽  
Vol 316 (5) ◽  
pp. H1124-H1140 ◽  
Author(s):  
Gabor A. Fulop ◽  
Stefano Tarantini ◽  
Andriy Yabluchanskiy ◽  
Andrea Molnar ◽  
Calin I. Prodan ◽  
...  
Keyword(s):  
Cognitive Impairment ◽  
Cerebral Arteries ◽  
Vascular Cognitive Impairment ◽  
Cerebral Veins ◽  
Older Individuals ◽  
Low Velocity ◽  
Venous Circulation ◽  
Age Related ◽  
The Brain

There has been an increasing appreciation of the role of vascular contributions to cognitive impairment and dementia (VCID) associated with old age. Strong preclinical and translational evidence links age-related dysfunction and structural alterations of the cerebral arteries, arterioles, and capillaries to the pathogenesis of many types of dementia in the elderly, including Alzheimer’s disease. The low-pressure, low-velocity, and large-volume venous circulation of the brain also plays critical roles in the maintenance of homeostasis in the central nervous system. Despite its physiological importance, the role of age-related alterations of the brain venous circulation in the pathogenesis of vascular cognitive impairment and dementia is much less understood. This overview discusses the role of cerebral veins in the pathogenesis of VCID. Pathophysiological consequences of age-related dysregulation of the cerebral venous circulation are explored, including blood-brain barrier disruption, neuroinflammation, exacerbation of neurodegeneration, development of cerebral microhemorrhages of venous origin, altered production of cerebrospinal fluid, impaired function of the glymphatics system, dysregulation of cerebral blood flow, and ischemic neuronal dysfunction and damage. Understanding the age-related functional and phenotypic alterations of the cerebral venous circulation is critical for developing new preventive, diagnostic, and therapeutic approaches to preserve brain health in older individuals.

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