Neurotransmitters, neuroreceptors and aging

Amenta, Francesco; Zaccheo, D; Collier, Wade L.

doi:10.1016/0047-6374(91)90059-9

Cited by 89 publications

(30 citation statements)

References 86 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…There is an age-dependent reduction in ␤-endorphin content and GABA synthesis in the lateral thalamus 14 and a decline in the concentration of gamma-aminobutyric and serotonin receptors. 15 Moreover, aging induces changes in all forms of perception, including vision, hearing, touch, sense, and proprioception. These changes result in difficulty in understanding, such as pain management methods like patient-controlled analgesia (PCA), communication such as pain assessment, and sensory and motor function such as per-ception of regional anesthesia.…”

Section: Physiological Changesmentioning

confidence: 99%

Management of Postoperative Analgesia in Elderly Patients

Aubrun

2005

Regional Anesthesia and Pain Medicine

View full text Add to dashboard Cite

Section: Physiological Changesmentioning

confidence: 99%

Management of Postoperative Analgesia in Elderly Patients

Aubrun

2005

Regional Anesthesia and Pain Medicine

View full text Add to dashboard Cite

“…Changes like loss of dendritic arborisation, neuronal death, and neurofibrillary abnormalities are found to occur in the cerebral cortex of aging individuals, including areas which are involved in nociceptive processing, like the prefrontal cortex, primary and secondary somatosensory cortex, anterior cingulate, hippocampus, thalamus, and insula [13]. The turnover and concentration of catecholamines [56] GABA [57] and opioid receptors [58] within the limbic system are found to be decreased, as well as serotonin receptor density [59], mainly within the prefrontal cortex and anterior cingulate [60].…”

Section: Physiological Changes With Agingmentioning

confidence: 99%

Effect of Age, Sex and Gender on Pain Sensitivity: A Narrative Review

Eltumi¹,

Tashani²

2017

TOPAINJ

View full text Add to dashboard Cite

Introduction:An increasing body of literature on sex and gender differences in pain sensitivity has been accumulated in recent years. There is also evidence from epidemiological research that painful conditions are more prevalent in older people. The aim of this narrative review is to critically appraise the relevant literature investigating the presence of age and sex differences in clinical and experimental pain conditions. Methods:A scoping search of the literature identifying relevant peer reviewed articles was conducted on May 2016. Information and evidence from the key articles were narratively described and data was quantitatively synthesised to identify gaps of knowledge in the research literature concerning age and sex differences in pain responses. Results:This critical appraisal of the literature suggests that the results of the experimental and clinical studies regarding age and sex differences in pain contain some contradictions as far as age differences in pain are concerned. While data from the clinical studies are more consistent and seem to point towards the fact that chronic pain prevalence increases in the elderly findings from the experimental studies on the other hand were inconsistent, with pain threshold increasing with age in some studies and decreasing with age in others. Conclusion:There is a need for further research using the latest advanced quantitative sensory testing protocols to measure the function of small nerve fibres that are involved in nociception and pain sensitivity across the human life span. Implications:Findings from these studies should feed into and inform evidence emerging from other types of studies (e.g. brain imaging technique and psychometrics) suggesting that pain in the older humans may have unique characteristics that affect how old patients respond to intervention.

show abstract

“…Since we have demonstrated that mAPP localizes in the nerve terminals of cholinergic neurons (38), one may hypothesize that APP interacts with the exocytotic machinery proteins of synaptic vesicles via X11L/ Mint-2. Since cholinergic neurotransmission is thought to be involved in learning and memory processes (52) and loss of function in cholinergic neurotransmission has been observed in senile dementia of AD (53), further characterization of X11L should increase our understanding of the physiological function of APP and the pathogenesis of sporadic type AD.…”

Section: Fig 10mentioning

confidence: 99%

Interaction of a Neuron-specific Protein Containing PDZ Domains with Alzheimer's Amyloid Precursor Protein

Tomita

Ozaki

Taru

et al. 1999

Journal of Biological Chemistry

144

225

View full text Add to dashboard Cite

Alzheimer's amyloid precursor protein (APP) 1 is an integral membrane protein with a receptor-like structure (1). A principal component of parenchymal amyloid deposits in Alzheimer's disease (AD) is ␤-amyloid (A␤) (2-4), which is derived from APP by proteolytic cleavage (1, 5-11). A␤ is thought to be generated through an intracellular protein secretory pathway of APP (for a review, see Ref. 12). The short APP cytoplasmic domain consisting of 47 amino acid residues is thought to be responsible for determination of APP metabolism (13-15) and possible signal transduction from a putative extracellular ligand that has yet to be identified (for a review, see Ref. 16). Because APP is a candidate pathogenic factor of AD, elucidation of the physiological function of APP as well as the determination of the metabolic mechanism of A␤ production should increase our understanding of the pathogenesis of AD. Using a yeast two-hybrid system, we isolated cDNA of proteins that interact with the cytoplasmic domain of APP (APP COOH ) in order to elucidate the molecular mechanisms of APP metabolism and function of APP. Previous efforts to identify and isolate proteins associating with APP COOH , utilizing the yeast two-hybrid system, have resulted in the isolation of proteins carrying phosphotyrosine binding/phosphotyrosine interaction (PI) domains such as Fe65 (17), 19), and X11 (20). The X11 gene, which is located on chromosome 9, was originally isolated as a gene candidate for Friedreich ataxia (21) and its partial cDNA was identified as a clone encoding a protein that associates with APP COOH (22). The PI domain of X11 interacts with the YENPTY motif of APP COOH (20). In the present study, we isolated a complete cDNA encoding an X11-like protein (X11L) from a human adult brain cDNA library, utilizing the yeast two-hybrid system and APP COOH as a bait. A partial short cDNA encoding approximately 190 amino acids in the PI domain of X11L has already been isolated using a similar procedure (22). However, detailed characterization of X11L binding to APP and identification of the role X11L plays in the physiological function of APP have not been performed. We found that human X11L requires a sequence containing the NPXY motif of APP COOH for APP binding and that association of the PI domain with APP was suppressed by a deletion of a amino-terminal domain fused to the PI domain (PI ϩ C construct) but enhanced by a deletion of a carboxyl-terminal domain fused to the PI domain (N ϩ PI construct). Co-transfection of full-length human X11L into cells that express stably transfected human APP695 cDNA resulted in decreased secretion of A␤40 but not A␤42. However, co-transfection into cells of the cDNA lacking the carboxyl-terminal domain (N ϩ PI construct) or a cDNA encoding only the PI domain (PI construct), whose protein products preserve the ability to bind to APP COOH , did not present the ability to modulate A␤ production. The present results suggest that the amino-terminal region of the PI domain is needed to regulate binding affinity...

show abstract

Neurotransmitters, neuroreceptors and aging

Cited by 89 publications

References 86 publications

Management of Postoperative Analgesia in Elderly Patients

Management of Postoperative Analgesia in Elderly Patients

Effect of Age, Sex and Gender on Pain Sensitivity: A Narrative Review

Interaction of a Neuron-specific Protein Containing PDZ Domains with Alzheimer's Amyloid Precursor Protein

Contact Info

Product

Resources

About