A Review of Biomarkers for Neurodegenerative Disease: Will They Swing Us Across the Valley?

Abstract Measures of the severity of cognitive impairment or parkinsonism are the usual endpoints in clinical trials for Alzheimer’s disease (AD) and Parkinson’s disease (PD), but are critically hampered by their lack of disease sensitivity and specificity. Due to the high failure rate of clinical t...
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Autor*in:	Beach, Thomas G. [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2017

Schlagwörter:	Blood Cerebrospinal fluid Clinical trial Diagnosis Etiology Pathogenesis Treatment

Übergeordnetes Werk:	Enthalten in: Neurology and Therapy - Berlin : Springer, 2012, 6(2017), Suppl 1 vom: Juli, Seite 5-13
Übergeordnetes Werk:	volume:6 ; year:2017 ; number:Suppl 1 ; month:07 ; pages:5-13

Links:	Volltext

DOI / URN:	10.1007/s40120-017-0072-x

Katalog-ID:	SPR032877137

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spelling	10.1007/s40120-017-0072-x doi (DE-627)SPR032877137 (SPR)s40120-017-0072-x-e DE-627 ger DE-627 rakwb eng 610 ASE Beach, Thomas G. verfasserin aut A Review of Biomarkers for Neurodegenerative Disease: Will They Swing Us Across the Valley? 2017 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Measures of the severity of cognitive impairment or parkinsonism are the usual endpoints in clinical trials for Alzheimer’s disease (AD) and Parkinson’s disease (PD), but are critically hampered by their lack of disease sensitivity and specificity. Due to the high failure rate of clinical trials, the rate of regulatory approval for efficacious new drugs has stagnated in the past few decades, with the gap between basic science discovery and clinical application metaphorically termed the “Valley of Death”. While the causes for this are probably multiple and complex, the usage of biomarkers as surrogate endpoints, particularly when they are molecularly-specific for the disease, has achieved some success in cancer trials, and it is likely that neurodegenerative disease trials would benefit from the same approach. As dementia and parkinsonism are not disease-specific clinical syndromes, both AD and PD trials have been flawed by reliance on clinical diagnosis and clinical endpoints. Clinical improvement has been a requirement for regulatory approval, but molecularly-specific biomarkers should improve both diagnostic accuracy and tracking of disease progression, allowing quicker screening of drug candidates. However, even when a molecularly-specific biomarker is found, such as amyloid imaging for AD, it may not reflect the entire extant molecular disease repertoire and may not serve equally well in the different roles of preclinical detection, diagnostic confirmation and surrogate endpoint, necessitating the usage of two, three or more biomarkers, deployed in series or in parallel. Blood (dpeaa)DE-He213 Cerebrospinal fluid (dpeaa)DE-He213 Clinical trial (dpeaa)DE-He213 Diagnosis (dpeaa)DE-He213 Etiology (dpeaa)DE-He213 Pathogenesis (dpeaa)DE-He213 Treatment (dpeaa)DE-He213 Enthalten in Neurology and Therapy Berlin : Springer, 2012 6(2017), Suppl 1 vom: Juli, Seite 5-13 (DE-627)726126209 (DE-600)2682228-3 2193-6536 nnns volume:6 year:2017 number:Suppl 1 month:07 pages:5-13 https://dx.doi.org/10.1007/s40120-017-0072-x kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 6 2017 Suppl 1 07 5-13
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allfieldsSound	10.1007/s40120-017-0072-x doi (DE-627)SPR032877137 (SPR)s40120-017-0072-x-e DE-627 ger DE-627 rakwb eng 610 ASE Beach, Thomas G. verfasserin aut A Review of Biomarkers for Neurodegenerative Disease: Will They Swing Us Across the Valley? 2017 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Measures of the severity of cognitive impairment or parkinsonism are the usual endpoints in clinical trials for Alzheimer’s disease (AD) and Parkinson’s disease (PD), but are critically hampered by their lack of disease sensitivity and specificity. Due to the high failure rate of clinical trials, the rate of regulatory approval for efficacious new drugs has stagnated in the past few decades, with the gap between basic science discovery and clinical application metaphorically termed the “Valley of Death”. While the causes for this are probably multiple and complex, the usage of biomarkers as surrogate endpoints, particularly when they are molecularly-specific for the disease, has achieved some success in cancer trials, and it is likely that neurodegenerative disease trials would benefit from the same approach. As dementia and parkinsonism are not disease-specific clinical syndromes, both AD and PD trials have been flawed by reliance on clinical diagnosis and clinical endpoints. Clinical improvement has been a requirement for regulatory approval, but molecularly-specific biomarkers should improve both diagnostic accuracy and tracking of disease progression, allowing quicker screening of drug candidates. However, even when a molecularly-specific biomarker is found, such as amyloid imaging for AD, it may not reflect the entire extant molecular disease repertoire and may not serve equally well in the different roles of preclinical detection, diagnostic confirmation and surrogate endpoint, necessitating the usage of two, three or more biomarkers, deployed in series or in parallel. Blood (dpeaa)DE-He213 Cerebrospinal fluid (dpeaa)DE-He213 Clinical trial (dpeaa)DE-He213 Diagnosis (dpeaa)DE-He213 Etiology (dpeaa)DE-He213 Pathogenesis (dpeaa)DE-He213 Treatment (dpeaa)DE-He213 Enthalten in Neurology and Therapy Berlin : Springer, 2012 6(2017), Suppl 1 vom: Juli, Seite 5-13 (DE-627)726126209 (DE-600)2682228-3 2193-6536 nnns volume:6 year:2017 number:Suppl 1 month:07 pages:5-13 https://dx.doi.org/10.1007/s40120-017-0072-x kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 6 2017 Suppl 1 07 5-13
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author	Beach, Thomas G.
spellingShingle	Beach, Thomas G. ddc 610 misc Blood misc Cerebrospinal fluid misc Clinical trial misc Diagnosis misc Etiology misc Pathogenesis misc Treatment A Review of Biomarkers for Neurodegenerative Disease: Will They Swing Us Across the Valley?
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title_sort	review of biomarkers for neurodegenerative disease: will they swing us across the valley?
title_auth	A Review of Biomarkers for Neurodegenerative Disease: Will They Swing Us Across the Valley?
abstract	Abstract Measures of the severity of cognitive impairment or parkinsonism are the usual endpoints in clinical trials for Alzheimer’s disease (AD) and Parkinson’s disease (PD), but are critically hampered by their lack of disease sensitivity and specificity. Due to the high failure rate of clinical trials, the rate of regulatory approval for efficacious new drugs has stagnated in the past few decades, with the gap between basic science discovery and clinical application metaphorically termed the “Valley of Death”. While the causes for this are probably multiple and complex, the usage of biomarkers as surrogate endpoints, particularly when they are molecularly-specific for the disease, has achieved some success in cancer trials, and it is likely that neurodegenerative disease trials would benefit from the same approach. As dementia and parkinsonism are not disease-specific clinical syndromes, both AD and PD trials have been flawed by reliance on clinical diagnosis and clinical endpoints. Clinical improvement has been a requirement for regulatory approval, but molecularly-specific biomarkers should improve both diagnostic accuracy and tracking of disease progression, allowing quicker screening of drug candidates. However, even when a molecularly-specific biomarker is found, such as amyloid imaging for AD, it may not reflect the entire extant molecular disease repertoire and may not serve equally well in the different roles of preclinical detection, diagnostic confirmation and surrogate endpoint, necessitating the usage of two, three or more biomarkers, deployed in series or in parallel.
abstractGer	Abstract Measures of the severity of cognitive impairment or parkinsonism are the usual endpoints in clinical trials for Alzheimer’s disease (AD) and Parkinson’s disease (PD), but are critically hampered by their lack of disease sensitivity and specificity. Due to the high failure rate of clinical trials, the rate of regulatory approval for efficacious new drugs has stagnated in the past few decades, with the gap between basic science discovery and clinical application metaphorically termed the “Valley of Death”. While the causes for this are probably multiple and complex, the usage of biomarkers as surrogate endpoints, particularly when they are molecularly-specific for the disease, has achieved some success in cancer trials, and it is likely that neurodegenerative disease trials would benefit from the same approach. As dementia and parkinsonism are not disease-specific clinical syndromes, both AD and PD trials have been flawed by reliance on clinical diagnosis and clinical endpoints. Clinical improvement has been a requirement for regulatory approval, but molecularly-specific biomarkers should improve both diagnostic accuracy and tracking of disease progression, allowing quicker screening of drug candidates. However, even when a molecularly-specific biomarker is found, such as amyloid imaging for AD, it may not reflect the entire extant molecular disease repertoire and may not serve equally well in the different roles of preclinical detection, diagnostic confirmation and surrogate endpoint, necessitating the usage of two, three or more biomarkers, deployed in series or in parallel.
abstract_unstemmed	Abstract Measures of the severity of cognitive impairment or parkinsonism are the usual endpoints in clinical trials for Alzheimer’s disease (AD) and Parkinson’s disease (PD), but are critically hampered by their lack of disease sensitivity and specificity. Due to the high failure rate of clinical trials, the rate of regulatory approval for efficacious new drugs has stagnated in the past few decades, with the gap between basic science discovery and clinical application metaphorically termed the “Valley of Death”. While the causes for this are probably multiple and complex, the usage of biomarkers as surrogate endpoints, particularly when they are molecularly-specific for the disease, has achieved some success in cancer trials, and it is likely that neurodegenerative disease trials would benefit from the same approach. As dementia and parkinsonism are not disease-specific clinical syndromes, both AD and PD trials have been flawed by reliance on clinical diagnosis and clinical endpoints. Clinical improvement has been a requirement for regulatory approval, but molecularly-specific biomarkers should improve both diagnostic accuracy and tracking of disease progression, allowing quicker screening of drug candidates. However, even when a molecularly-specific biomarker is found, such as amyloid imaging for AD, it may not reflect the entire extant molecular disease repertoire and may not serve equally well in the different roles of preclinical detection, diagnostic confirmation and surrogate endpoint, necessitating the usage of two, three or more biomarkers, deployed in series or in parallel.
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