scholarly journals The Executive Control of Face Memory

2011 ◽  
Vol 24 (4) ◽  
pp. 285-298 ◽  
Author(s):  
Steven Z. Rapcsak ◽  
Emily C. Edmonds
Keyword(s):  
Frontal Lobe ◽  
Source Memory ◽  
Source Monitoring ◽  
Facial Recognition ◽  
Critical Role ◽  
Functional Decline ◽  
Memory Systems ◽  
Face Memory ◽  
Age Related ◽  
Constructive Process

Patients with frontal lobe damage and cognitively normal elderly individuals demonstrate increased susceptibility to false facial recognition. In this paper we review neuropsychological evidence consistent with the notion that the common functional impairment underlying face memory distortions in both subject populations is a context recollection/source monitoring deficit, coupled with excessive reliance on relatively preserved facial familiarity signals in recognition decisions. In particular, we suggest that due to the breakdown of strategic memory retrieval, monitoring, and decision operations, individuals with frontal lobe impairment caused by focal damage or age-related functional decline do not have a reliable mechanism for attributing the experience of familiarity to the correct context or source. Memory illusions are mostly apparent under conditions of uncertainty when the face cue does not directly elicit relevant identity-specific contextual information, leaving the source of familiarity unspecified or ambiguous. Based on these findings, we propose that remembering faces is a constructive process that requires dynamic interactions between temporal lobe memory systems that operate in an automatic or bottom-up fashion and frontal executive systems that provide strategic top-down control of recollection. Executive memory control functions implemented by prefrontal cortex play a critical role in suppressing false facial recognition and related source memory misattributions.

scholarly journals Procyanidin C1 is a natural agent with senolytic activity against aging and age-related diseases

2021 ◽  
Author(s):  
Qixia Xu ◽  
Qiang Fu ◽  
Zi Li ◽  
Hanxin Liu ◽  
Ying Wang ◽  
...  
Keyword(s):  
Life Stage ◽  
Critical Role ◽  
Functional Decline ◽  
Grape Seed ◽  
Multiple Organs ◽  
Age Related ◽  
Physical Dysfunction ◽  
Natural Product Library ◽  
Enhancing Production ◽  
And Control

Abstract Aging causes functional decline of multiple organs and increases the risk of age-related pathologies. In advanced lives, accumulation of senescent cells, which develop the senescence-associated secretory phenotype (SASP), promotes chronic inflammation and causes diverse conditions. Here we report the frontline outcome of screening a natural product library with human primary stromal cells as an experimental model. Multiple candidate compounds were assayed, and grape seed extract (GSE) was selected for further investigation due to its leading capacity in targeting senescent cells. We found procyanidin C1 (PCC1), a polyphenolic component, plays a critical role in mediating the antiaging effects of GSE. PCC1 blocks the SASP expression when used at low concentrations. Importantly, it selectively kills senescent cells upon application at higher concentrations, mainly by enhancing production of reactive oxygen species (ROS) and disturbing mitochondrial membrane potential, processes accompanied by upregulation of Bcl-2 family pro-apoptotic factors Puma and Noxa in senescent cells. PCC1 depletes senescent cells in treatment-damaged tumor microenvironment (TME) and enhances therapeutic efficacy when combined with chemotherapy in preclinical assays. Intermittent administration of PCC1 to both senescent cell-implanted mice and naturally aged animals alleviated physical dysfunction and prolonged post-treatment survival, thus providing substantial benefits in late life stage. Together, our study identifies PCC1 as a distinct natural senolytic agent, which may be exploited to delay aging and control age-related pathologies in future medicine.

scholarly journals Procyanidin C1 is a natural agent with senolytic activity against aging and age-related diseases

2021 ◽  
Author(s):  
Qixia Xu ◽  
Qiang Fu ◽  
Zi Li ◽  
Hanxin Liu ◽  
Ying Wang ◽  
...  
Keyword(s):  
Life Stage ◽  
Critical Role ◽  
Functional Decline ◽  
Grape Seed ◽  
Multiple Organs ◽  
Age Related ◽  
Physical Dysfunction ◽  
Natural Product Library ◽  
Enhancing Production ◽  
And Control

AbstractAging causes functional decline of multiple organs and increases the risk of age-related pathologies. In advanced lives, accumulation of senescent cells, which develop the senescence-associated secretory phenotype (SASP), promotes chronic inflammation and causes diverse conditions. Here we report the frontline outcome of screening a natural product library with human primary stromal cells as an experimental model. Multiple candidate compounds were assayed, and grape seed extract (GSE) was selected for further investigation due to its leading capacity in targeting senescent cells. We found procyanidin C1 (PCC1), a polyphenolic component, plays a critical role in mediating the antiaging effects of GSE. PCC1 blocks the SASP expression when used at low concentrations. Importantly, it selectively kills senescent cells upon application at higher concentrations, mainly by enhancing production of reactive oxygen species (ROS) and disturbing mitochondrial membrane potential, processes accompanied by upregulation of Bcl-2 family pro-apoptotic factors Puma and Noxa in senescent cells. PCC1 depletes senescent cells in treatment-damaged tumor microenvironment (TME) and enhances therapeutic efficacy when combined with chemotherapy in preclinical assays. Intermittent administration of PCC1 to both senescent cell-implanted mice and naturally aged animals alleviated physical dysfunction and prolonged post-treatment survival, thus providing substantial benefits in late life stage. Together, our study identifies PCC1 as a distinct natural senolytic agent, which may be exploited to delay aging and control age-related pathologies in future medicine.

A Reexamination of Source Monitoring Deficits in the Elderly: Evidence for Independent Age Deficits of Item and Source Memory

2004 ◽  
Vol 5 (2) ◽  
pp. 138-144 ◽  
Author(s):  
J.J. Tree ◽  
T.J. Perfect
Keyword(s):  
Source Memory ◽  
Source Monitoring ◽  
Memory Performance ◽  
Correct Recall ◽  
The Elderly ◽  
Item Information ◽  
Source Information ◽  
Substantial Evidence ◽  
Age Related ◽  
Age Deficits

AbstractWithin the experimental literature there is substantial evidence of larger age-related deficits in retrieving source information relative to item-based information. However, this evidence is potentially subject to methodological criticism given that several studies have argued for the presence of source-monitoring deficits by examining source memory contingent on correct recall of item information but not the reverse. In order to address this potential shortcoming our study examines recall of both item information contingent on correct source judgement and source-based information contingent on correct recall of item information. We demonstrate that when this novel type of analysis is conducted, there are age deficits for both source and item information, and no evidence of a selectively greater source-monitoring deficit in the elderly. The results are discussed with reference to two overarching theoretical positions concerning age-related deficits in memory performance.

Perceptual Effects and Recollective Experience in Face Recognition

2005 ◽  
Vol 52 (3) ◽  
pp. 224-231 ◽  
Author(s):  
Chrisanthi Nega
Keyword(s):  
Face Recognition ◽  
Recognition Memory ◽  
Congruency Effect ◽  
Facial Recognition ◽  
Memory Systems ◽  
Study Time ◽  
Perceptual Fluency ◽  
Recollective Experience ◽  
Trace Strength ◽  
Size Congruency

Abstract. Four experiments were conducted investigating the effect of size congruency on facial recognition memory, measured by remember, know and guess responses. Different study times were employed, that is extremely short (300 and 700 ms), short (1,000 ms), and long times (5,000 ms). With the short study time (1,000 ms) size congruency occurred in knowing. With the long study time the effect of size congruency occurred in remembering. These results support the distinctiveness/fluency account of remembering and knowing as well as the memory systems account, since the size congruency effect that occurred in knowing under conditions that facilitated perceptual fluency also occurred independently in remembering under conditions that facilitated elaborative encoding. They do not support the idea that remember and know responses reflect differences in trace strength.

Multidimensional source monitoring: Prior retrieval of one source attribute improves source memory for a second

2010 ◽  
Author(s):  
Michael R. Dewitt ◽  
Justin B. Knight ◽  
B. Hunter Ball ◽  
Jason L. Hicks
Keyword(s):  
Source Memory ◽  
Source Monitoring

The Role of Glyoxalase in Glycation and Carbonyl Stress Induced Metabolic Disorders

2020 ◽  
Vol 21 (9) ◽  
pp. 846-859
Author(s):  
Mohd Saeed ◽  
Mohd Adnan Kausar ◽  
Rajeev Singh ◽  
Arif J. Siddiqui ◽  
Asma Akhter
Keyword(s):  
Protein Misfolding ◽  
Covalent Binding ◽  
Critical Role ◽  
Enzymatic Reaction ◽  
Treatment Strategies ◽  
Bioactive Molecules ◽  
Carbonyl Stress ◽  
Defense System ◽  
Pathological Conditions ◽  
Age Related

Glycation refers to the covalent binding of sugar molecules to macromolecules, such as DNA, proteins, and lipids in a non-enzymatic reaction, resulting in the formation of irreversibly bound products known as advanced glycation end products (AGEs). AGEs are synthesized in high amounts both in pathological conditions, such as diabetes and under physiological conditions resulting in aging. The body’s anti-glycation defense mechanisms play a critical role in removing glycated products. However, if this defense system fails, AGEs start accumulating, which results in pathological conditions. Studies have been shown that increased accumulation of AGEs acts as key mediators in multiple diseases, such as diabetes, obesity, arthritis, cancer, atherosclerosis, decreased skin elasticity, male erectile dysfunction, pulmonary fibrosis, aging, and Alzheimer’s disease. Furthermore, glycation of nucleotides, proteins, and phospholipids by α-oxoaldehyde metabolites, such as glyoxal (GO) and methylglyoxal (MGO), causes potential damage to the genome, proteome, and lipidome. Glyoxalase-1 (GLO-1) acts as a part of the anti-glycation defense system by carrying out detoxification of GO and MGO. It has been demonstrated that GLO-1 protects dicarbonyl modifications of the proteome and lipidome, thereby impeding the cell signaling and affecting age-related diseases. Its relationship with detoxification and anti-glycation defense is well established. Glycation of proteins by MGO and GO results in protein misfolding, thereby affecting their structure and function. These findings provide evidence for the rationale that the functional modulation of the GLO pathway could be used as a potential therapeutic target. In the present review, we summarized the newly emerged literature on the GLO pathway, including enzymes regulating the process. In addition, we described small bioactive molecules with the potential to modulate the GLO pathway, thereby providing a basis for the development of new treatment strategies against age-related complications.

Molecular Mechanisms of Complement System Proteins and Matrix Metalloproteinases in the Pathogenesis of Age-Related Macular Degeneration

2019 ◽  
Vol 19 (10) ◽  
pp. 705-718 ◽  
Author(s):  
Naima Mansoor ◽  
Fazli Wahid ◽  
Maleeha Azam ◽  
Khadim Shah ◽  
Anneke I. den Hollander ◽  
...  
Keyword(s):  
Matrix Metalloproteinases ◽  
Macular Degeneration ◽  
Complement System ◽  
Molecular Mechanisms ◽  
Critical Role ◽  
Age Related Macular Degeneration ◽  
Genetic Changes ◽  
Complement System Proteins ◽  
Age Related ◽  
Common Genetic Variants

: Age-related macular degeneration (AMD) is an eye disorder affecting predominantly the older people above the age of 50 years in which the macular region of the retina deteriorates, resulting in the loss of central vision. The key factors associated with the pathogenesis of AMD are age, smoking, dietary, and genetic risk factors. There are few associated and plausible genes involved in AMD pathogenesis. Common genetic variants (with a minor allele frequency of >5% in the population) near the complement genes explain 40–60% of the heritability of AMD. The complement system is a group of proteins that work together to destroy foreign invaders, trigger inflammation, and remove debris from cells and tissues. Genetic changes in and around several complement system genes, including the CFH, contribute to the formation of drusen and progression of AMD. Similarly, Matrix metalloproteinases (MMPs) that are normally involved in tissue remodeling also play a critical role in the pathogenesis of AMD. MMPs are involved in the degradation of cell debris and lipid deposits beneath retina but with age their functions get affected and result in the drusen formation, succeeding to macular degeneration. In this review, AMD pathology, existing knowledge about the normal and pathological role of complement system proteins and MMPs in the eye is reviewed. The scattered data of complement system proteins, MMPs, drusenogenesis, and lipofusogenesis have been gathered and discussed in detail. This might add new dimensions to the understanding of molecular mechanisms of AMD pathophysiology and might help in finding new therapeutic options for AMD.

Pathogenesis of Age-related Cataract: a systematic review of proteomic studies

2020 ◽  
Vol 17 ◽  
Author(s):  
Christina Karakosta ◽  
Argyrios Tzamalis ◽  
Michalis Aivaliotis ◽  
Ioannis Tsinopoulos
Keyword(s):  
Systematic Review ◽  
Oxidant Stress ◽  
Critical Role ◽  
Human Lens ◽  
Nuclear Cataract ◽  
Cataract Formation ◽  
Post Translational Modification ◽  
Ability To Act ◽  
Age Related

Background/Objective:: The aim of this systematic review is to identify all the available data on human lens proteomics with a critical role to age-related cataract formation in order to elucidate the physiopathology of the aging lens. Materials and Methods:: We searched on Medline and Cochrane databases. The search generated 328 manuscripts. We included nine original proteomic studies that investigated human cataractous lenses. Results:: Deamidation was the major age-related post-translational modification. There was a significant increase in the amount of αA-crystallin D-isoAsp58 present at all ages, while an increase in the extent of Trp oxidation was apparent in cataract lenses when compared to aged normal lenses. During aging, enzymes with oxidized cysteine at critical sites included GAPDH, glutathione synthase, aldehyde dehydrogenase, sorbitol dehydrogenase, and PARK7. Conclusion:: D-isoAsp in αA crystallin could be associated with the development of age-related cataract in human, by contributing to the denaturation of a crystallin, and decreasing its ability to act as a chaperone. Oxidation of Trp may be associated with nuclear cataract formation in human, while the role of oxidant stress in age-related cataract formation is dominant.

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