Abstract
Drug discovery efforts in Alzheimer’s disease (AD) have been directed in the last ten years to develop “disease-modifying drugs” able to exert neuroprotective effects in an early phase of AD pathogenesis. Unfortunately several candidate disease-modifying drugs have failed in Phase III clinical trials conducted in mild to moderate AD for different methodological difficulties, such as the time course of treatment in relation to development of disease as well as the appropriate use of validated biological and neuropsychological markers. Mild cognitive impairment (MCI) has been considered a precursor of AD. Much effort is now directed to identify the most appropriate and sensitive markers which can predict the progression from MCI to AD, such as neuroimaging markers (e.g. hippocampal atrophy and amyloid positron emission tomography imaging), cerebrospinal fluid markers (i.e. association of elevated tau with low levels of amyloid β -peptide(1-42) and neuropsychological markers (i.e. episodic memory deficits and executive dysfunction). Recent studies demonstrate that the combination of these different biomarkers significantly increases the chance to predict the conversion into AD within 24 months. These biomarkers will be essential in the future to analyze clinical efficacy of disease-modifying drugs in MCI patients at high risk to develop AD. In the present review we analyze recent evidence on the combination of neuropsychological and biological markers in AD as a new tool to track disease progression in early AD as well as the response to disease-modifying drugs.
Keywords: Alzheimer’s disease, biological markers, disease-modifying drugs, mild cognitive impairment, neuropsychological tests, risk factors.
CNS & Neurological Disorders - Drug Targets
Title:Searching for Disease-Modifying Drugs in AD: Can We Combine Neuropsychological Tools with Biological Markers?
Volume: 13 Issue: 1
Author(s): Filippo Caraci, Sabrina Castellano, Salvatore Salomone, Filippo Drago, Paolo Bosco and Santo Di Nuovo
Affiliation:
Keywords: Alzheimer’s disease, biological markers, disease-modifying drugs, mild cognitive impairment, neuropsychological tests, risk factors.
Abstract: Drug discovery efforts in Alzheimer’s disease (AD) have been directed in the last ten years to develop “disease-modifying drugs” able to exert neuroprotective effects in an early phase of AD pathogenesis. Unfortunately several candidate disease-modifying drugs have failed in Phase III clinical trials conducted in mild to moderate AD for different methodological difficulties, such as the time course of treatment in relation to development of disease as well as the appropriate use of validated biological and neuropsychological markers. Mild cognitive impairment (MCI) has been considered a precursor of AD. Much effort is now directed to identify the most appropriate and sensitive markers which can predict the progression from MCI to AD, such as neuroimaging markers (e.g. hippocampal atrophy and amyloid positron emission tomography imaging), cerebrospinal fluid markers (i.e. association of elevated tau with low levels of amyloid β -peptide(1-42) and neuropsychological markers (i.e. episodic memory deficits and executive dysfunction). Recent studies demonstrate that the combination of these different biomarkers significantly increases the chance to predict the conversion into AD within 24 months. These biomarkers will be essential in the future to analyze clinical efficacy of disease-modifying drugs in MCI patients at high risk to develop AD. In the present review we analyze recent evidence on the combination of neuropsychological and biological markers in AD as a new tool to track disease progression in early AD as well as the response to disease-modifying drugs.
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Cite this article as:
Caraci Filippo, Castellano Sabrina, Salomone Salvatore, Drago Filippo, Bosco Paolo and Nuovo Di Santo, Searching for Disease-Modifying Drugs in AD: Can We Combine Neuropsychological Tools with Biological Markers?, CNS & Neurological Disorders - Drug Targets 2014; 13 (1) . https://dx.doi.org/10.2174/18715273113129990103
DOI https://dx.doi.org/10.2174/18715273113129990103 |
Print ISSN 1871-5273 |
Publisher Name Bentham Science Publisher |
Online ISSN 1996-3181 |
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