scholarly journals Functional Implications of Changes in the Senescent Brain: A Review

1978 ◽  
Vol 5 (4) ◽  
pp. 417-424 ◽  
Author(s):  
Charles H.M. Beck
Keyword(s):  
Old Age ◽  
Cognitive Processing ◽  
Memory Trace ◽  
Physiological Changes ◽  
Age Related ◽  
Dopaminergic Systems ◽  
Functional Implications ◽  
The Brain

SUMMARY:The morphological, chemical, and physiological changes in the brain accompanying old age are reviewed. The deterioration of the striatal and hypothalamic dopaminergic systems were implicated in the onset of age related Parkinsonian-like slowing of performance and altered affect. Cholinergic hippocampal and neocortical systems were chemically and physiologically abnormal in the aged. The implications for slowed cognitive processing and persistance of the memory trace are presented.

scholarly journals Age-Related Changes in Human and Nonhuman Timing

2017 ◽  
Vol 5 (3-4) ◽  
pp. 261-279 ◽  
Author(s):  
Rannie Xu ◽  
Russell M. Church
Keyword(s):  
Time Perception ◽  
Cognitive Processing ◽  
Cognitive Aging ◽  
Comparative Research ◽  
Biochemical Changes ◽  
Age Related ◽  
Timing Ability ◽  
The Many ◽  
The Brain ◽  
Age Related Changes

The capacity for timed behavior is ubiquitous across the animal kingdom, making time perception an ideal topic of comparative research across human and nonhuman subjects. One of the many consequences of normal aging is a systematic decline in timing ability, often accompanied by a host of behavioral and biochemical changes in the brain. In this review, we describe some of these behavioral and biochemical changes in human and nonhuman subjects. Given the involvement of timing in higher-order cognitive processing, age-related changes in timing ability can act as a marker for cognitive decline in older adults. Finally, we offer a comparison between human and nonhuman timing through the perspective of Alzheimer’s disease. Taken together, we suggest that understanding timing functions and dysfunctions can improve theoretical accounts of cognitive aging and time perception, and the use of nonhuman subjects constitutes an integral part of this process.

Old age psychiatry

2019 ◽  
pp. 541-564
Author(s):  
David Semple ◽  
Roger Smyth
Keyword(s):  
Old Age ◽  
Elder Abuse ◽  
The Elderly ◽  
Power Of Attorney ◽  
Advanced Directives ◽  
Psychiatric Illnesses ◽  
Age Related ◽  
Old Age Psychiatry ◽  
Ageing Patient ◽  
The Brain

This chapter covers old age psychiatry, including both psychiatric illnesses in older people and specific aspects of illness with regard to the elderly, from neuroses and psychoses to mood disorders. New disorders owing to specific old age-related issues, such as bereavement, isolation, and the changing physiology of the brain, are covered, as well as pre-existing illnesses in the ageing patient. The increasing recognition of elder abuse is defined, and responses outlined. End of life considerations, such as power of attorney and advanced directives, are included.

Changes of the Brain Synapses During Aging. New Aspects

2001 ◽  
Vol 56 (11-12) ◽  
pp. 921-929 ◽  
Author(s):  
Kleopatra Schulpis ◽  
Artemis Doulgeraki ◽  
Stylianos Tsakiris
Keyword(s):  
Successful Aging ◽  
Brain Aging ◽  
Aging Brain ◽  
Compensatory Mechanisms ◽  
Age Related ◽  
Adaptive Mechanisms ◽  
Functional Implications ◽  
Effects Of Aging ◽  
The Brain

Abstract The process of brain aging is an interaction of age-related losses and compensatory mechanisms. This review is focused on the changes of the synaptic number and structure, their functional implications, regarding neurotransmission, as well as the electrical activity of neuronal circuits. Moreover, the importance of calcium homeostasis is strongly emphasized. It is also suggested that many neuronal properties are preserved, as a result of adaptive mechanisms, and that a series of interdependent factors regulate brain aging. The "new fron­ tier" in research is the challenge of understanding the effects of aging, both to prevent degen­ erative diseases and reduce their consequences. New aspects are considered a) the role of nitric oxide, b) free radicals and apoptosis, c) impaired cerebral microcirculation, d) m eta­ bolic features of aging brain, e) the possible neuroprotective role of insulin-like growth factor-1 (IGF-1) and ovarian steroids and e) stress and aging. These numerous multifactorial approaches are essential to understand the process of aging. The more we learn about it, the more we realize how to achieve "successful" aging. M inireview

Potential immunotherapy for Alzheimer disease and age-related dementia

2019 ◽  
Vol 21 (1) ◽  
pp. 21-25 ◽  
Keyword(s):  
Immune System ◽  
Alzheimer Disease ◽  
Cross Talk ◽  
Immune Checkpoint ◽  
Short Review ◽  
Immune Checkpoint Blockade ◽  
Checkpoint Blockade ◽  
New Approach ◽  
Age Related ◽  
The Brain

Emerging results support the concept that Alzheimer disease (AD) and age-related dementia are affected by the ability of the immune system to contain the brain's pathology. Accordingly, well-controlled boosting, rather than suppression of systemic immunity, has been suggested as a new approach to modify disease pathology without directly targeting any of the brain's disease hallmarks. Here, we provide a short review of the mechanisms orchestrating the cross-talk between the brain and the immune system. We then discuss how immune checkpoint blockade directed against the PD-1/PD-L1 pathways could be developed as an immunotherapeutic approach to combat this disease using a regimen that will address the needs to combat AD.

Potential immunotherapy for Alzheimer disease and age-related dementia

2019 ◽  
Vol 21 (1) ◽  
pp. 21-25 ◽  
Keyword(s):  
Immune System ◽  
Alzheimer Disease ◽  
Cross Talk ◽  
Immune Checkpoint ◽  
Short Review ◽  
Immune Checkpoint Blockade ◽  
Checkpoint Blockade ◽  
New Approach ◽  
Age Related ◽  
The Brain

Emerging results support the concept that Alzheimer disease (AD) and age-related dementia are affected by the ability of the immune system to contain the brain’s pathology. Accordingly, well-controlled boosting, rather than suppression of systemic immunity, has been suggested as a new approach to modify disease pathology without directly targeting any of the brain’s disease hallmarks. Here, we provide a short review of the mechanisms orchestrating the cross-talk between the brain and the immune system. We then discuss how immune checkpoint blockade directed against the PD-1/PD-L1 pathways could be developed as an immunotherapeutic approach to combat this disease using a regimen that will address the needs to combat AD.

scholarly journals Corticobasal Degeneration Misdiagnosed As Musculoskeletal Disease: A Challenging Diagnosis of Higher-Level Gait Disease

2020 ◽  
Vol 11 (04) ◽  
pp. 640-642
Author(s):  
Halil Onder
Keyword(s):  
Corticobasal Degeneration ◽  
The Elderly ◽  
Gait Disorders ◽  
Physiological Changes ◽  
Gait Abnormality ◽  
Age Related ◽  
Musculoskeletal Problems ◽  
Neurological Exam ◽  
Long Time ◽  
High Level

AbstractGait disorders are common in the elderly as there are various causes of neurological and non-neurological conditions. On the other hand, most of the gait parameters do change with advancing age which is identified as age-related physiological changes in gait. At this point, the discrimination between age-related physiological changes and gait disorders may be strictly challenging. After identifying gait as an abnormal pattern, classification of it and making the responsible pathophysiology also require high-level expertise in this regard. Herein, we present a rare patient with corticobasal degeneration (CBD) who had admitted initially due to complaints of gait problems. Over a long time, the patient had received the misdiagnosis of gait abnormality due to musculoskeletal problems by multiple physicians. However, the detailed neurological exam showed a higher level gait disorder (HLGD). Further investigations at this point yielded the diagnosis of CBD.

scholarly journals Probable Causes of Alzheimer’s Disease

Sci ◽  
2021 ◽  
Vol 3 (1) ◽  
pp. 16
Author(s):  
James David Adams
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Lactic Acid ◽  
Blood Brain Barrier ◽  
Transient Receptor Potential ◽  
Brain Barrier ◽  
Folate Intake ◽  
Blood Brain ◽  
Age Related ◽  
The Brain

A three-part mechanism is proposed for the induction of Alzheimer’s disease: (1) decreased blood lactic acid; (2) increased blood ceramide and adipokines; (3) decreased blood folic acid. The age-related nature of these mechanisms comes from age-associated decreased muscle mass, increased visceral fat and changes in diet. This mechanism also explains why many people do not develop Alzheimer’s disease. Simple changes in lifestyle and diet can prevent Alzheimer’s disease. Alzheimer’s disease is caused by a cascade of events that culminates in damage to the blood–brain barrier and damage to neurons. The blood–brain barrier keeps toxic molecules out of the brain and retains essential molecules in the brain. Lactic acid is a nutrient to the brain and is produced by exercise. Damage to endothelial cells and pericytes by inadequate lactic acid leads to blood–brain barrier damage and brain damage. Inadequate folate intake and oxidative stress induced by activation of transient receptor potential cation channels and endothelial nitric oxide synthase damage the blood–brain barrier. NAD depletion due to inadequate intake of nicotinamide and alterations in the kynurenine pathway damages neurons. Changes in microRNA levels may be the terminal events that cause neuronal death leading to Alzheimer’s disease. A new mechanism of Alzheimer’s disease induction is presented involving lactic acid, ceramide, IL-1β, tumor necrosis factor α, folate, nicotinamide, kynurenine metabolites and microRNA.

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