Pub Date : 2023-06-16DOI: 10.1016/j.bionps.2023.100068
Jana Harenbrock , Heinz Holling , Graham Reid , Ivan Koychev
Sleep has an important role for long-term memory consolidation. As deficits in learning and memory are clinical characteristics of Alzheimer’s disease (AD), it has been suggested that disruptions in sleep-mediated consolidation processes are related to AD. Indeed, sleep disruptions and sleep disorders are often comorbid with AD and perhaps precede the onset of AD symptoms as a risk factor. Additionally, research has shown that sleep disruptions and disorders are associated with accumulation of β-amyloid (AB), a neuropathologic hallmark and biomarker of AD. However, the studies that have investigated the relationship between sleep disturbances and AB burden have been heterogenous in design and quality, leaving it unclear whether the overall effect is statistically significant. As such, this paper investigated the relationship between sleep disturbances and AB burden by meta-analytically integrating reported correlations that have been published to date. Results revealed that higher levels of cerebral AB (lower AB42/40 ratios) were related to shorter sleep durations, highlighting the importance of total sleep time in supporting the clearance of AB during slow-wave sleep. Herein we also controlled for heterogeneity in the included studies by conducting several moderator analyses, showing an important role for age, sex, cognitive impairment, sleep disorders, and education in influencing the associations between sleep disturbances and AB.
{"title":"A meta-analysis of the relationship between sleep and β-Amyloid biomarkers in Alzheimer’s disease","authors":"Jana Harenbrock , Heinz Holling , Graham Reid , Ivan Koychev","doi":"10.1016/j.bionps.2023.100068","DOIUrl":"https://doi.org/10.1016/j.bionps.2023.100068","url":null,"abstract":"<div><p>Sleep has an important role for long-term memory consolidation. As deficits in learning and memory are clinical characteristics of Alzheimer’s disease (AD), it has been suggested that disruptions in sleep-mediated consolidation processes are related to AD. Indeed, sleep disruptions and sleep disorders are often comorbid with AD and perhaps precede the onset of AD symptoms as a risk factor. Additionally, research has shown that sleep disruptions and disorders are associated with accumulation of β-amyloid (AB), a neuropathologic hallmark and biomarker of AD. However, the studies that have investigated the relationship between sleep disturbances and AB burden have been heterogenous in design and quality, leaving it unclear whether the overall effect is statistically significant. As such, this paper investigated the relationship between sleep disturbances and AB burden by meta-analytically integrating reported correlations that have been published to date. Results revealed that higher levels of cerebral AB (lower AB42/40 ratios) were related to shorter sleep durations, highlighting the importance of total sleep time in supporting the clearance of AB during slow-wave sleep. Herein we also controlled for heterogeneity in the included studies by conducting several moderator analyses, showing an important role for age, sex, cognitive impairment, sleep disorders, and education in influencing the associations between sleep disturbances and AB.</p></div>","PeriodicalId":52767,"journal":{"name":"Biomarkers in Neuropsychiatry","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2023-06-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"50187063","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2023-06-01DOI: 10.1016/j.bionps.2022.100060
Serhiy Y. Chumachenko , Molly McVoy
Background
As the need for prompt identification and management of childhood mood. disorders continues to grow, increasing interest has shifted towards potential objective. biomarkers. One modality that has shown promise as a biomarker has been quantitative electroencephalography or qEEG. In this review, we expand on our previous investigation into qEEG biomarker research for child mood disorders and potential challenges faced in ongoing development.
Ongoing research into qEEG:
Since our last systematic review, qEEG biomarker research of childhood major depressive disorder remained sparse, with only one novel awake qEEG investigation in children despite ongoing adult depression qEEG research. For bipolar disorder, previously identified qEEG researchers have continued investigation into Bipolar II diagnosis identification, Bipolar I versus II diagnostic discrimination, and general bipolar biomarker utilization.
Challenges faced by qEEG:
While the nature of qEEG as a data-driven, easily performed, and easily analyzable biomarker is promising, challenges to clinical utilization remain, including direct anatomical correlation and generation of patientfacing clinically tested and usable tools. However, preliminary general utilization of qEEG in clinical settings with childhood mood disorder has shown excellent efficacy, and ongoing research to address these limitations is feasible and ongoing.
Conclusions
While qEEG biomarker research in child mood disorders has remained slow, there is a clear need and strong ongoing potential for future investigations.
{"title":"A narrative review and discussion of concepts and ongoing data regarding quantitative EEG as a childhood mood disorder biomarker","authors":"Serhiy Y. Chumachenko , Molly McVoy","doi":"10.1016/j.bionps.2022.100060","DOIUrl":"https://doi.org/10.1016/j.bionps.2022.100060","url":null,"abstract":"<div><h3>Background</h3><p>As the need for prompt identification and management of childhood mood. disorders continues to grow, increasing interest has shifted towards potential objective. biomarkers. One modality that has shown promise as a biomarker has been quantitative electroencephalography or qEEG. In this review, we expand on our previous investigation into qEEG biomarker research for child mood disorders and potential challenges faced in ongoing development.</p></div><div><h3>Ongoing research into qEEG:</h3><p>Since our last systematic review, qEEG biomarker research of childhood major depressive disorder remained sparse, with only one novel awake qEEG investigation in children despite ongoing adult depression qEEG research. For bipolar disorder, previously identified qEEG researchers have continued investigation into Bipolar II diagnosis identification, Bipolar I versus II diagnostic discrimination, and general bipolar biomarker utilization.</p></div><div><h3>Challenges faced by qEEG:</h3><p>While the nature of qEEG as a data-driven, easily performed, and easily analyzable biomarker is promising, challenges to clinical utilization remain, including direct anatomical correlation and generation of patientfacing clinically tested and usable tools. However, preliminary general utilization of qEEG in clinical settings with childhood mood disorder has shown excellent efficacy, and ongoing research to address these limitations is feasible and ongoing.</p></div><div><h3>Conclusions</h3><p>While qEEG biomarker research in child mood disorders has remained slow, there is a clear need and strong ongoing potential for future investigations.</p></div>","PeriodicalId":52767,"journal":{"name":"Biomarkers in Neuropsychiatry","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2023-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"50190117","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Frontotemporal dementia (FTD) is one of the most common neurodegenerative diseases, encompassing a myriad of different, clinically distinct subtypes which all target the frontoinsular region. FTD is characterized by a decline in behavioral, language, and executive functions. Due to its proximity to similar diseases, both in symptomology and mechanism, FTD remains challenging to diagnose conclusively. As a result, searching for distinct biomarkers that allow clinicians to differentiate between FTD and other neurocognitive disorders is extremely important. This review examines studies published in the past decade to evaluate which current biomarkers are the most clinically viable and where future research might lead. Genetic screening for FTD, specifically the three most common mutations to the TDP-43, MAPT, and PGRN genes, show promising predictive ability and could help patients access treatment in the early stages of the disease. In addition, serum and CSF biomarkers can help clinicians track the disease process and show good specificity when differentiating between FTD, primary psychiatric disorders, and other neurodegenerative diseases, especially when coupled with imaging techniques such as MRI and PET. Lastly, recent advances in machine learning may allow future researchers and clinicians to comprehensively analyze FTD's biochemical and imaging fingerprint, leading to increasingly accurate and timely diagnosis. Further work must be focused on transitioning the understanding of FTD biomarkers from research to concrete tools available to clinicians and patients, with the hopes of advancing the quality of care available to those suffering from FTD.
{"title":"Biomarkers in frontotemporal dementia: Current landscape and future directions","authors":"Abbott Gifford , Nathan Praschan , Amy Newhouse , Zeina Chemali","doi":"10.1016/j.bionps.2023.100065","DOIUrl":"10.1016/j.bionps.2023.100065","url":null,"abstract":"<div><p>Frontotemporal dementia (FTD) is one of the most common neurodegenerative diseases, encompassing a myriad of different, clinically distinct subtypes which all target the frontoinsular region. FTD is characterized by a decline in behavioral, language, and executive functions. Due to its proximity to similar diseases, both in symptomology and mechanism, FTD remains challenging to diagnose conclusively. As a result, searching for distinct biomarkers that allow clinicians to differentiate between FTD and other neurocognitive disorders is extremely important. This review examines studies published in the past decade to evaluate which current biomarkers are the most clinically viable and where future research might lead. Genetic screening for FTD, specifically the three most common mutations to the TDP-43, MAPT, and PGRN genes, show promising predictive ability and could help patients access treatment in the early stages of the disease. In addition, serum and CSF biomarkers can help clinicians track the disease process and show good specificity when differentiating between FTD, primary psychiatric disorders, and other neurodegenerative diseases, especially when coupled with imaging techniques such as MRI and PET. Lastly, recent advances in machine learning may allow future researchers and clinicians to comprehensively analyze FTD's biochemical and imaging fingerprint, leading to increasingly accurate and timely diagnosis. Further work must be focused on transitioning the understanding of FTD biomarkers from research to concrete tools available to clinicians and patients, with the hopes of advancing the quality of care available to those suffering from FTD.</p></div>","PeriodicalId":52767,"journal":{"name":"Biomarkers in Neuropsychiatry","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2023-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"44262302","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2023-06-01DOI: 10.1016/j.bionps.2023.100067
Maísa Braga Aguiar, Gabriela Haas Henrique Barros, Gisele W.B. Colleoni, Maysa Seabra Cendoroglo, Clineu de Mello Almada Filho
Systemic inflammatory processes can cause changes in cognition and functional capacity in the general population. Currently there are no accessible biomarkers capable of early detection and monitoring of such pathologies, and only few studies involving older than 80 years-old population were done. The C-reactive protein (CRP) and blood counts are low-cost tests that are often performed in routine basis. From the blood counts it is possible to evaluate the absolute count of neutrophils and lymphocytes, which are peripheral blood inflammatory markers. With these results, it is also possible to evaluate the neutrophils to lymphocytes ratio (NLR). Therefore, these tests may be potential biomarkers in the evaluation of the development of dementia, mild cognitive disorder, and functional dependence, with the possibility of assisting in the clinical management and prevention of such pathologies.
Objective
To evaluate the association between cognition and functional capacity with C-reactive protein, absolute neutrophil count, lymphocyte count, and NLR in a population of elderly people aged 80 years and older.
Methods
Observational analytical cross-sectional study conducted in the cohort of the Longevous Project of the Discipline of Geriatrics and Gerontology of UNIFESP. Complete blood counts (CBC) and CRP were collected from 244 patients included in the study between 2010 and 2013. Gender and the presence of hypertension and diabetes mellitus were also characterized. Associations between the absolute values of neutrophils and lymphocytes and the NLR with cognitive tests (mini mental state examination, MMSE, and clock drawing test, CDT) and with functional capacity (basic activities of daily living, BADL or Katz score, and instrumental activities of daily living, IADL or Lawton score) were performed using nonparametric Mann-Whitney and Kruskall-Wallis statistical tests.
Results
We found no associations between the markers obtained by the CBC and the cognitive assessment tests. We also found no association between the CRP and the MMSE. However, we obtained a statistically significant difference between the CRP marker and the CDT, with P = 0.003. There was no statistically significant difference between markers obtained by CBC or CRP with the BADLs. But we observed a statistically significant association between the IADLs and the absolute count of neutrophils and lymphocytes, respectively P = 0.0379 and 0.0190.
Conclusion
The presented results contribute to the hypothesis that serum inflammatory biomarkers can be useful in the assessment of health outcomes. We identified that patients with lower functional capacity for IADLs have higher absolute neutrophil and lymphocyte counts when compared to patients with higher functional capacity. In addition, we identified that patients with low performance on CDT have CRP at higher levels when compared to patie
{"title":"Association between C-reactive protein, neutrophils, lymphocytes, cognition, and functional capacity in an oldest old population","authors":"Maísa Braga Aguiar, Gabriela Haas Henrique Barros, Gisele W.B. Colleoni, Maysa Seabra Cendoroglo, Clineu de Mello Almada Filho","doi":"10.1016/j.bionps.2023.100067","DOIUrl":"10.1016/j.bionps.2023.100067","url":null,"abstract":"<div><p>Systemic inflammatory processes can cause changes in cognition and functional capacity in the general population. Currently there are no accessible biomarkers capable of early detection and monitoring of such pathologies, and only few studies involving older than 80 years-old population were done. The C-reactive protein (CRP) and blood counts are low-cost tests that are often performed in routine basis. From the blood counts it is possible to evaluate the absolute count of neutrophils and lymphocytes, which are peripheral blood inflammatory markers. With these results, it is also possible to evaluate the neutrophils to lymphocytes ratio (NLR). Therefore, these tests may be potential biomarkers in the evaluation of the development of dementia, mild cognitive disorder, and functional dependence, with the possibility of assisting in the clinical management and prevention of such pathologies.</p></div><div><h3>Objective</h3><p>To evaluate the association between cognition and functional capacity with C-reactive protein, absolute neutrophil count, lymphocyte count, and NLR in a population of elderly people aged 80 years and older.</p></div><div><h3>Methods</h3><p>Observational analytical cross-sectional study conducted in the cohort of the Longevous Project of the Discipline of Geriatrics and Gerontology of UNIFESP. Complete blood counts (CBC) and CRP were collected from 244 patients included in the study between 2010 and 2013. Gender and the presence of hypertension and diabetes mellitus were also characterized. Associations between the absolute values of neutrophils and lymphocytes and the NLR with cognitive tests (mini mental state examination, MMSE, and clock drawing test, CDT) and with functional capacity (basic activities of daily living, BADL or Katz score, and instrumental activities of daily living, IADL or Lawton score) were performed using nonparametric Mann-Whitney and Kruskall-Wallis statistical tests.</p></div><div><h3>Results</h3><p>We found no associations between the markers obtained by the CBC and the cognitive assessment tests. We also found no association between the CRP and the MMSE. However, we obtained a statistically significant difference between the CRP marker and the CDT, with P = 0.003. There was no statistically significant difference between markers obtained by CBC or CRP with the BADLs. But we observed a statistically significant association between the IADLs and the absolute count of neutrophils and lymphocytes, respectively P = 0.0379 and 0.0190.</p></div><div><h3>Conclusion</h3><p>The presented results contribute to the hypothesis that serum inflammatory biomarkers can be useful in the assessment of health outcomes. We identified that patients with lower functional capacity for IADLs have higher absolute neutrophil and lymphocyte counts when compared to patients with higher functional capacity. In addition, we identified that patients with low performance on CDT have CRP at higher levels when compared to patie","PeriodicalId":52767,"journal":{"name":"Biomarkers in Neuropsychiatry","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2023-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"42759522","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2023-06-01DOI: 10.1016/j.bionps.2023.100062
Matthew Luebke , Manisha Parulekar , Florian P. Thomas
In this review, we evaluate the role of fluid biomarkers related to neurodegenerative diseases. Such conditions present diagnostic challenges due to phenotypic heterogeneity, longitudinal evolution, overlap between diagnostic entities, and variability in progression. Biomarkers can potentially provide insight into diagnosis, progression, prognostication, and treatment efficacy. This review covers recent advances in fluid biomarkers including beta-amyloid, tau protein, neurofilament light chain, alpha-synuclein and glial fibrillary protein, and briefly touches upon imaging biomarkers. For each biomarker, we discuss the pathophysiological correlates, clinical uses, accuracy, and limitations.
{"title":"Fluid biomarkers for the diagnosis of neurodegenerative diseases","authors":"Matthew Luebke , Manisha Parulekar , Florian P. Thomas","doi":"10.1016/j.bionps.2023.100062","DOIUrl":"10.1016/j.bionps.2023.100062","url":null,"abstract":"<div><p>In this review, we evaluate the role of fluid biomarkers related to neurodegenerative diseases. Such conditions present diagnostic challenges due to phenotypic heterogeneity, longitudinal evolution, overlap between diagnostic entities, and variability in progression. Biomarkers can potentially provide insight into diagnosis, progression, prognostication, and treatment efficacy. This review covers recent advances in fluid biomarkers including beta-amyloid, tau protein, neurofilament light chain, alpha-synuclein and glial fibrillary protein, and briefly touches upon imaging biomarkers. For each biomarker, we discuss the pathophysiological correlates, clinical uses, accuracy, and limitations.</p></div>","PeriodicalId":52767,"journal":{"name":"Biomarkers in Neuropsychiatry","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2023-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41573218","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2023-06-01DOI: 10.1016/j.bionps.2023.100066
Jennifer Abi Gerges , Issam Chalhoub , Carl Atallah , Rita Khoury
Chronic traumatic encephalopathy (CTE) is a progressive neurodegenerative condition that occurs several years following repetitive mild concussive or sub concussive brain injuries. To date, it is a post-mortem diagnosis. Traumatic encephalopathy syndrome (TES) is a framework that was developed as a clinical predictor of CTE in living individuals. Development of biomarkers of CTE, detectable through imaging or bodily fluids will aid improve the diagnostic accuracy of CTE in life, and help develop prevention and therapeutic strategies. This article reviews biomarkers investigated to date, and discusses challenges and future avenues in this burgeoning field.
{"title":"Biomarkers of chronic traumatic encephalopathy: A state-of-the art review","authors":"Jennifer Abi Gerges , Issam Chalhoub , Carl Atallah , Rita Khoury","doi":"10.1016/j.bionps.2023.100066","DOIUrl":"10.1016/j.bionps.2023.100066","url":null,"abstract":"<div><p>Chronic traumatic encephalopathy (CTE) is a progressive neurodegenerative condition that occurs several years following repetitive mild concussive or sub concussive brain injuries. To date, it is a post-mortem diagnosis. Traumatic encephalopathy syndrome (TES) is a framework that was developed as a clinical predictor of CTE in living individuals. Development of biomarkers of CTE, detectable through imaging or bodily fluids will aid improve the diagnostic accuracy of CTE in life, and help develop prevention and therapeutic strategies. This article reviews biomarkers investigated to date, and discusses challenges and future avenues in this burgeoning field.</p></div>","PeriodicalId":52767,"journal":{"name":"Biomarkers in Neuropsychiatry","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2023-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"45978084","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2023-06-01DOI: 10.1016/j.bionps.2023.100064
Walaa G. El Sheikh , Bshara Sleem , Firas Kobeissy , Maya Bizri
Delirium is a neuropsychiatric disorder highly prevalent in the intensive care unit (ICU), especially among elderly patients. Symptoms develop suddenly over a short period of time in the form of a fluctuating mental state marked by severe inattention and disturbance in cognition. Dementia, on the other hand, develops over a long period of time as a result of a neurodegenerative disorder. In this review, we aim to identify overlapping biomarkers between delirium and dementia to have a better understanding of the underlying pathophysiological mechanisms relating these two disorders. Overlapping biomarkers included low levels of albumin and IGF-1, a presence of the APOE ε4 allele (APOE ε4 +), as well as higher levels of of AβN-40, S100β, procalcitonin, IL-1β, NfL, prolactin, creatinine, MMP-9, and homocysteine. We put forward several hypotheses on the convergence of the pathophysiology of these two disorders. It is plausible that ICU-acquired delirium arises as a sign of prodromal dementia or as a result of chronic systemic inflammation and concomitant neuroinflammation due to an increase in S100β proteins in the brain as a byproduct of chronic glial activation. Simultaneously, accumulation of creatinine may render the functioning of the kidneys sub-optimal, which can have deleterious effects on cognitive functioning, while lower serum albumin can increase the risk of Aβ accumulation in the brain and therefore increase the likelihood of delirium and future dementia. Moreover, homozygosity in the APOE ε4 allele coupled with elevated plasma CRP might increase the risk of delirium and trigger the onset of Alzheimer’s disease (AD). Therapeutic approaches targeting the above biomarkers need to be the subject of further investigation, especially among those exhibiting persistent delirium.
{"title":"Biomarkers of delirium and relation to dementia among the elderly in the intensive care unit: A narrative review","authors":"Walaa G. El Sheikh , Bshara Sleem , Firas Kobeissy , Maya Bizri","doi":"10.1016/j.bionps.2023.100064","DOIUrl":"https://doi.org/10.1016/j.bionps.2023.100064","url":null,"abstract":"<div><p>Delirium is a neuropsychiatric disorder highly prevalent in the intensive care unit (ICU), especially among elderly patients. Symptoms develop suddenly over a short period of time in the form of a fluctuating mental state marked by severe inattention and disturbance in cognition. Dementia, on the other hand, develops over a long period of time as a result of a neurodegenerative disorder. In this review, we aim to identify overlapping biomarkers between delirium and dementia to have a better understanding of the underlying pathophysiological mechanisms relating these two disorders. Overlapping biomarkers included low levels of albumin and IGF-1, a presence of the APOE ε4 allele (APOE ε4 +), as well as higher levels of of AβN-40, S100β, procalcitonin, IL-1β, NfL, prolactin, creatinine, MMP-9, and homocysteine. We put forward several hypotheses on the convergence of the pathophysiology of these two disorders. It is plausible that ICU-acquired delirium arises as a sign of prodromal dementia or as a result of chronic systemic inflammation and concomitant neuroinflammation due to an increase in S100β proteins in the brain as a byproduct of chronic glial activation. Simultaneously, accumulation of creatinine may render the functioning of the kidneys sub-optimal, which can have deleterious effects on cognitive functioning, while lower serum albumin can increase the risk of Aβ accumulation in the brain and therefore increase the likelihood of delirium and future dementia. Moreover, homozygosity in the APOE ε4 allele coupled with elevated plasma CRP might increase the risk of delirium and trigger the onset of Alzheimer’s disease (AD). Therapeutic approaches targeting the above biomarkers need to be the subject of further investigation, especially among those exhibiting persistent delirium.</p></div>","PeriodicalId":52767,"journal":{"name":"Biomarkers in Neuropsychiatry","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2023-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"50190107","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2023-06-01DOI: 10.1016/j.bionps.2023.100063
Joanna E. Georgakas , Matthew D. Howe , Louisa I. Thompson , Natalie M. Riera , Meghan C. Riddle
Alzheimer’s disease (AD) is an age-related neurodegenerative disease and the leading cause of dementia worldwide. AD is associated with several neuropathologic changes including the progressive accumulation of extracellular amyloid-β (Aβ) plaques, intracellular neurofibrillary tau tangles, neuroinflammation, cerebral small vessel disease and neurodegeneration, many of which are known to begin years before the onset of clinical symptoms. As such, there is a growing interest in developing biomarkers that can be used to detect these changes in the brains of at-risk individuals to facilitate earlier and more accurate diagnosis. This may allow for earlier intervention with disease-modifying therapies to slow the progression of irreversible neurodegeneration and improve quality of life. The current review seeks to provide a concise overview of the neuropathology and genetics underlying AD, and then summarize the most promising clinically available and experimental biomarkers of AD. These include structural neuroimaging, functional magnetic resonance imaging (fMRI), positron emission tomography (PET), cerebrospinal fluid (CSF), and blood-based assays. Multiple potential clinical uses for these biomarkers are then described, including screening at-risk populations for disease, aiding in differential diagnosis of dementia and mild cognitive impairment (MCI), monitoring the impact of lifestyle intervention and disease modifying therapies, identification and treatment of neuropsychiatric symptoms of dementia, and aiding in planning for end of life care. Finally, additional areas of future research are discussed, including replication of biomarker studies in more diverse patient cohorts, characterization of real-world clinical and psychological impacts of biomarker testing, as well as novel biomarkers currently under investigation.
{"title":"Biomarkers of Alzheimer’s disease: Past, present and future clinical use","authors":"Joanna E. Georgakas , Matthew D. Howe , Louisa I. Thompson , Natalie M. Riera , Meghan C. Riddle","doi":"10.1016/j.bionps.2023.100063","DOIUrl":"10.1016/j.bionps.2023.100063","url":null,"abstract":"<div><p>Alzheimer’s disease (AD) is an age-related neurodegenerative disease and the leading cause of dementia worldwide. AD is associated with several neuropathologic changes including the progressive accumulation of extracellular amyloid-β (Aβ) plaques, intracellular neurofibrillary tau tangles, neuroinflammation, cerebral small vessel disease and neurodegeneration, many of which are known to begin years before the onset of clinical symptoms. As such, there is a growing interest in developing biomarkers that can be used to detect these changes in the brains of at-risk individuals to facilitate earlier and more accurate diagnosis. This may allow for earlier intervention with disease-modifying therapies to slow the progression of irreversible neurodegeneration and improve quality of life. The current review seeks to provide a concise overview of the neuropathology and genetics underlying AD, and then summarize the most promising clinically available and experimental biomarkers of AD. These include structural neuroimaging, functional magnetic resonance imaging (fMRI), positron emission tomography (PET), cerebrospinal fluid (CSF), and blood-based assays. Multiple potential clinical uses for these biomarkers are then described, including screening at-risk populations for disease, aiding in differential diagnosis of dementia and mild cognitive impairment (MCI), monitoring the impact of lifestyle intervention and disease modifying therapies, identification and treatment of neuropsychiatric symptoms of dementia, and aiding in planning for end of life care. Finally, additional areas of future research are discussed, including replication of biomarker studies in more diverse patient cohorts, characterization of real-world clinical and psychological impacts of biomarker testing, as well as novel biomarkers currently under investigation.</p></div>","PeriodicalId":52767,"journal":{"name":"Biomarkers in Neuropsychiatry","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2023-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"44083470","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2022-12-01DOI: 10.1016/j.bionps.2022.100056
Danny Perez Sierra , Ashutosh Tripathi , Anilkumar Pillai
Complement system is one of the most important defense mechanisms of the innate immune system. In addition to their roles in immune regulation, complement proteins are also involved in neurodevelopment and adult brain plasticity. Complement dysregulation has been shown in neurodevelopmental disorders including schizophrenia and autism spectrum disorder as well as in mood disorders. A number of clinical as well as genetic studies suggest the role of complement proteins in the cortical thinning and excessive synaptic pruning frequently associated with schizophrenia. The changes in complement proteins are also associated with the pathophysiology of autism spectrum disorder, major depressive disorder and bipolar disorder, but warrant further research. In addition, rodent models suggest a strong case for complement system in anxiety-like behavior. In this article, we review the recent findings on the role of complement system in neuropsychiatric disorders. The possible uses for future complement targeted therapies are also discussed.
{"title":"Dysregulation of complement system in neuropsychiatric disorders: A mini review","authors":"Danny Perez Sierra , Ashutosh Tripathi , Anilkumar Pillai","doi":"10.1016/j.bionps.2022.100056","DOIUrl":"10.1016/j.bionps.2022.100056","url":null,"abstract":"<div><p>Complement system is one of the most important defense mechanisms of the innate immune system. In addition to their roles in immune regulation, complement proteins are also involved in neurodevelopment and adult brain plasticity. Complement dysregulation has been shown in neurodevelopmental disorders including schizophrenia and autism spectrum disorder as well as in mood disorders. A number of clinical as well as genetic studies suggest the role of complement proteins in the cortical thinning and excessive synaptic pruning frequently associated with schizophrenia. The changes in complement proteins are also associated with the pathophysiology of autism spectrum disorder, major depressive disorder and bipolar disorder, but warrant further research. In addition, rodent models suggest a strong case for complement system in anxiety-like behavior. In this article, we review the recent findings on the role of complement system in neuropsychiatric disorders. The possible uses for future complement targeted therapies are also discussed.</p></div>","PeriodicalId":52767,"journal":{"name":"Biomarkers in Neuropsychiatry","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2022-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/6c/38/nihms-1855846.PMC10136364.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9399673","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2022-12-01DOI: 10.1016/j.bionps.2022.100058
Amir Levine , Jeffrey R. Strawn
Extracellular vesicles (EVs) are tiny (<1 µm) membrane-bound vesicles released by all tissues (including the brain) that cross the blood-brain barrier and facilitate cell-to-cell communication within and among tissues. They represent the body’s “Twitter system,” rapidly disseminating packets of information throughout the brain and body. Not unlike Twitter, EVs convey short messages through their cargos (e.g., RNAs, proteins, lipids, and metabolites), which direct the molecular activity of recipient cells in both health and disease. Extracellular vesicles serve as mediators of brain function and represent a reservoir for CNS-specific biomarkers that can be sequestered from plasma to guide diagnosis and treatment, representing a new frontier in the molecular study of psychiatric illness and in the development of biomarkers. The EV field has immense potential to revolutionize diagnostic approaches in psychiatry, facilitate precision treatment, predict response, and discover much-needed novel therapeutics.
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