Is dopamine involved in Alzheimer's disease?

被引:220
作者
Martorana, Alessandro [1 ,2 ]
Koch, Giacomo [1 ,2 ]
机构
[1] Univ Roma Tor Vergata, Syst Med Dept, Clin Neurol Memory Clin, I-00133 Rome, Italy
[2] Santa Lucia Fdn IRCCS, Dept Behav & Clin Neurol, Non Invas Brain Stimulat Unit, Rome, Italy
关键词
Alzheimer's disease; dopamine; alpha 7-nicotinic receptor; extrapyramidal signs; apathy; NICOTINIC ACETYLCHOLINE-RECEPTOR; AMYLOID PRECURSOR PROTEIN; EXTRAPYRAMIDAL SIGNS; COGNITIVE IMPAIRMENT; SUBSTANTIA-NIGRA; NEUROFIBRILLARY CHANGES; CORTICAL EXCITABILITY; TRANSGENIC MICE; CSF BIOMARKERS; BETA;
D O I
10.3389/fnagi.2014.00252
中图分类号
R592 [老年病学]; C [社会科学总论];
学科分类号
03 ; 0303 ; 100203 ;
摘要
Alzheimer's Disease (AD) is a neurodegenerative disorder characterized by progressive cognitive decline and dementia. Recent advances indicate that AD pathogenesis appears more complex than its mere neuropathology. Changes in synaptic plasticity, neuronal disarray and cell death are pathways commonly recognized as pathogenic mechanisms of AD. It is thought that the altered metabolism of certain membrane proteins may lead to the production of amyloid (A beta) oligomers that are characterized by an highly toxic effect on neurotransmission pathways, such as those mediated by Acetylcholine. The interaction of A beta oligomers with these neurotansmitters systems would in turn induce cell dysfunction, neurotransmitters signaling imbalance and finally lead to the appearance of neurological signs. In this perspective, it is still debated how and if these mechanisms may also engage the dopaminergic system in AD. Recent experimental work revealed that the dopaminergic system may well be involved in the occurrence of cognitive decline, often being predictive of rapidly progressive forms of AD. However, a clear idea on the role of the dopamine system in AD is still missing. Here we review the more recent evidences supporting the notion that the dopaminergic dysfunction has a pathogenic role in cognitive decline symptoms of AD.
引用
收藏
页数:6
相关论文
共 70 条
[1]   A non-α7 nicotinic acetylcholine receptor modulates excitatory input to hippocampal CA1 interneurons [J].
Alkondon, M ;
Albuquerque, EX .
JOURNAL OF NEUROPHYSIOLOGY, 2002, 87 (03) :1651-1654
[2]   LOSS OF DOPAMINE UPTAKE SITES LABELED WITH [H-3] GBR-12935 IN ALZHEIMERS-DISEASE [J].
ALLARD, P ;
ALAFUZOFF, I ;
CARLSSON, A ;
ERIKSSON, K ;
ERICSON, E ;
GOTTFRIES, CG ;
MARCUSSON, JO .
EUROPEAN NEUROLOGY, 1990, 30 (04) :181-185
[3]   Levodopa ameliorates learning and memory deficits in a murine model of Alzheimer's disease [J].
Ambree, Oliver ;
Richter, Helene ;
Sachser, Norbert ;
Lewejohann, Lars ;
Dere, Ekrem ;
Silva, Maria Angelica de Souza ;
Herring, Arne ;
Keyvani, Kathy ;
Paulus, Werner ;
Schaebitz, Wolf-Ruediger .
NEUROBIOLOGY OF AGING, 2009, 30 (08) :1192-1204
[4]   Tau and α-synuclein brainstem pathology in Alzheimer disease:: relation with extrapyramidal signs [J].
Attems, Johannes ;
Quass, Magdalena ;
Jellinger, Kurt A. .
ACTA NEUROPATHOLOGICA, 2007, 113 (01) :53-62
[5]   The relationship between subcortical tau pathology and Alzheimer's disease [J].
Attems, Johannes ;
Thal, Dietmar R. ;
Jellinger, Kurt A. .
BIOCHEMICAL SOCIETY TRANSACTIONS, 2012, 40 :711-715
[6]   Linking cognitive aging to alterations in dopamine neurotransmitter functioning: Recent data and future avenues [J].
Backman, Lars ;
Lindenberger, Ulman ;
Li, Shu-Chen ;
Nyberg, Lars .
NEUROSCIENCE AND BIOBEHAVIORAL REVIEWS, 2010, 34 (05) :670-677
[7]   Amyloid-β Associated Cortical Thinning in Clinically Normal Elderly [J].
Becker, J. Alex ;
Hedden, Trey ;
Carmasin, Jeremy ;
Maye, Jacqueline ;
Rentz, Dorene M. ;
Putcha, Deepti ;
Fischl, Bruce ;
Greve, Douglas N. ;
Marshall, Gad A. ;
Salloway, Stephen ;
Marks, Donald ;
Buckner, Randy L. ;
Sperling, Reisa A. ;
Johnson, Keith A. .
ANNALS OF NEUROLOGY, 2011, 69 (06) :1032-1042
[8]   Living on the edge with too many mouths to feed: Why dopamine neurons die [J].
Bolam, J. Paul ;
Pissadaki, Eleftheria K. .
MOVEMENT DISORDERS, 2012, 27 (12) :1478-1483
[9]   ALZHEIMERS-DISEASE - STRIATAL AMYLOID DEPOSITS AND NEUROFIBRILLARY CHANGES [J].
BRAAK, H ;
BRAAK, E .
JOURNAL OF NEUROPATHOLOGY AND EXPERIMENTAL NEUROLOGY, 1990, 49 (03) :215-224
[10]   The pathology of the substantia nigra in Alzheimer disease with extrapyramidal signs [J].
Burns, JM ;
Galvin, JE ;
Roe, CM ;
Morris, JC ;
McKeel, DW .
NEUROLOGY, 2005, 64 (08) :1397-1403