Up to the present, the identification of neurochemical alterations underlying Alzheimer's disease allowed for the development of the first generation of therapies that are somewhat specific for this disorder. Although both cholinesterase inhibitors and NMDA receptor blockade have well-proven efficacy levels, the clinical outcomes of patients receiving such treatments are rather limited; with many authors considering them as "symptomatic" treatments. In this context, it is safe to say that although the microscopic alterations present in AD have been well known for over a century, we have failed to identify therapeutic agents able to block the synthesis and aggregation of amyloid beta 42 or the formation of neurofibrillary tangles. Some new therapeutic strategies have however been explored in the last few years. This paper aimed at reviewing the evidence supporting these new "disease modifying" therapeutic options, including anti-amyloid and anti-Tau strategies. Copyright (C) 2017, Taiwan Society of Geriatric Emergency & Critical Care Medicine. Published by Elsevier Taiwan LLC.
机构:
Department of Neurology, Institute of Psychological Medicine and Clinical Neuroscience, Cardiff University, CardiffDepartment of Neurology, Institute of Psychological Medicine and Clinical Neuroscience, Cardiff University, Cardiff
Peall K.J.
Robertson N.P.
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Department of Neurology, Institute of Psychological Medicine and Clinical Neuroscience, Cardiff University, CardiffDepartment of Neurology, Institute of Psychological Medicine and Clinical Neuroscience, Cardiff University, Cardiff
机构:
Wayne State Univ, Sch Med, Dept Neurosurg, 540 E Canfield St, Detroit, MI 48201 USAWayne State Univ, Sch Med, Dept Neurosurg, 540 E Canfield St, Detroit, MI 48201 USA
机构:
Univ Szeged, Fac Med, Albert Szent Gyorgyi Clin Ctr, Dept Neurol, H-6725 Szeged, HungaryUniv Szeged, Fac Med, Albert Szent Gyorgyi Clin Ctr, Dept Neurol, H-6725 Szeged, Hungary
Zadori, Denes
Veres, Gabor
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Univ Szeged, Fac Med, Albert Szent Gyorgyi Clin Ctr, Dept Neurol, H-6725 Szeged, HungaryUniv Szeged, Fac Med, Albert Szent Gyorgyi Clin Ctr, Dept Neurol, H-6725 Szeged, Hungary
Veres, Gabor
Szalardy, Levente
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Univ Szeged, Fac Med, Albert Szent Gyorgyi Clin Ctr, Dept Neurol, H-6725 Szeged, HungaryUniv Szeged, Fac Med, Albert Szent Gyorgyi Clin Ctr, Dept Neurol, H-6725 Szeged, Hungary
Szalardy, Levente
Klivenyi, Peter
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Univ Szeged, Fac Med, Albert Szent Gyorgyi Clin Ctr, Dept Neurol, H-6725 Szeged, HungaryUniv Szeged, Fac Med, Albert Szent Gyorgyi Clin Ctr, Dept Neurol, H-6725 Szeged, Hungary
Klivenyi, Peter
Toldi, Jozsef
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Univ Szeged, Fac Sci & Informat, Dept Physiol Anat & Neurosci, H-6725 Szeged, Hungary
MTA SZTE Neurosci Res Grp, Szeged, HungaryUniv Szeged, Fac Med, Albert Szent Gyorgyi Clin Ctr, Dept Neurol, H-6725 Szeged, Hungary
Toldi, Jozsef
Vecsei, Laszlo
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Univ Szeged, Fac Med, Albert Szent Gyorgyi Clin Ctr, Dept Neurol, H-6725 Szeged, Hungary
MTA SZTE Neurosci Res Grp, Szeged, HungaryUniv Szeged, Fac Med, Albert Szent Gyorgyi Clin Ctr, Dept Neurol, H-6725 Szeged, Hungary