Nicotinic receptor abnormalities in Alzheimer’s disease

Court, Jennifer A.; Martin-Ruiz, Carmen; Piggott, Margaret A.; Spurden, Dean; Griffiths, Martin; Perry, Elaine K.

doi:10.1016/s0006-3223(00)01116-1

Cited by 209 publications

(152 citation statements)

References 64 publications

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“…Significantly reduced 5-[ 125 I]-A-85380 binding in AD compared to controls was also found in the entorhinal cortex, consistent with reports of deficits in [ 3 H]nicotine binding (Court et al, 2001) and [ 3 H]epibatidine binding and a4 subunit protein expression in the neocortex in AD (Martin-Ruiz et al, 1999;Guan et al, 2000). A trend of lower 5-[ 125 I]-A-85380 in thalamic nuclei was seen in AD; however, this did not reach statistical significance confirming earlier reports of no major deficits in thalamic areas in AD (Xuereb et al, 1990;Court et al, 2001 (Perry et al, 1995;MartinRuiz et al, 2000). The relative severity of the reduction of [ 3 H]epibatidine binding in the temporal cortex has been reported to be related to disturbances in consciousness (DOC) seen in some DLB patients, where patients with DOC show higher binding in the temporal cortex, including the entorhinal cortex, than patients showing no DOC (Ballard et al, 2002).…”

Section: Disease Comparisonssupporting

confidence: 88%

“…It may be that these striatal nAChRs deficits are responsible for disorders of movement observed in late stages of AD (Court et al, 2000a). Significantly reduced 5-[ 125 I]-A-85380 binding in AD compared to controls was also found in the entorhinal cortex, consistent with reports of deficits in [ 3 H]nicotine binding (Court et al, 2001) and [ 3 H]epibatidine binding and a4 subunit protein expression in the neocortex in AD (Martin-Ruiz et al, 1999;Guan et al, 2000). A trend of lower 5-[ 125 I]-A-85380 in thalamic nuclei was seen in AD; however, this did not reach statistical significance confirming earlier reports of no major deficits in thalamic areas in AD (Xuereb et al, 1990;Court et al, 2001 (Perry et al, 1995;MartinRuiz et al, 2000).…”

Section: Disease Comparisonssupporting

confidence: 86%

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Nicotinic Acetylcholine Receptor Distribution in Alzheimer's Disease, Dementia with Lewy Bodies, Parkinson's Disease, and Vascular Dementia: In Vitro Binding Study Using 5-[125I]-A-85380

Pimlott

Piggott

Owens

et al. 2003

Neuropsychopharmacol

152

105

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Section: Disease Comparisonssupporting

confidence: 88%

Section: Disease Comparisonssupporting

confidence: 86%

Nicotinic Acetylcholine Receptor Distribution in Alzheimer's Disease, Dementia with Lewy Bodies, Parkinson's Disease, and Vascular Dementia: In Vitro Binding Study Using 5-[125I]-A-85380

Pimlott

Piggott

Owens

et al. 2003

Neuropsychopharmacol

152

105

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“…In particular, cholinergic nicotinic receptors were found to be reduced in 30-40%, mainly due to reduction of the α 4 β 2 subtype, with relative preservation of the α 7 -nicotinic receptors (Court et al, 2001;Perry et al, 1995). Thus, α 7 -nicotinic receptors can be considered useful for studying the possibility of memory recovery.…”

Section: Discussionmentioning

confidence: 99%

Choline reverses scopolamine-induced memory impairment by improving memory reconsolidation

Blake

Boccia

Krawczyk

et al. 2012

Neurobiology of Learning and Memory

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Please cite this article as: Blake, M.G., Boccia, M.M., Krawczyk, M.C., Delorenzi, A., Baratti, C.M., Choline reverses scopolamine-induced memory impairment by improving memory reconsolidation, Neurobiology of Learning and Memory (2012), doi: http://dx.doi. org/10.1016/j.nlm.2012.07.001 This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. were not subjected to memory reactivation, suggesting that the performance effects are not due to non-specific effects of the drug. The effects of Ch also depended on the age of the reactivated memory. Altogether, our results suggest that Ch exerts its effects by modulating memory reconsolidation, and that the memory impairment induced by low doses of SCP is a memory expression failure and not a storage deficit. Therefore, reconsolidation, among other functions, might serve to change memory expression in later tests. Summarizing, our results open new avenues about the behavioral significance and the physiological functions of memory reconsolidation, providing new strategies for recovering memories from some types of amnesia. Research highlights-Pre-training administration of scopolamine leads to memory impairment.-Intra-hippocampal administration of choline modulates memory reconsolidation -Choline reverses scopolamine-induced amnesia by enhancing memory reconsolidation -Low doses of scopolamine cause memory expression deficit, but not storage impairment -Reconsolidation could modify the ability of a memory for being expressed later

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“…For the reasons enumerated herein, neuronal nAChRs were among the most likely targets for KYNA's actions in the brain. First, changes in KYNA often parallel alterations in nAChR function/expression in a number of neurologic disorders (Perry et al, 1990;Hellstrom-Lindahl et al, 1999;Freedman et al, 2000;Court et al, 2001). Second, similarly to NMDA receptors, nAChRs are involved in regulating neuronal plasticity (Albuquerque et al, 1997;Broide and Leslie, 1999;Mansvelder and McGehee, 2000;Ji et al, 2001) and survival in the brain (Zoli et al, 1999;Kihara et al, 2001).…”

Section: Kynurenic Acid (Kyna)mentioning

confidence: 99%

“…Over the past 10 years, there has been a remarkable expansion in research on the therapeutic potential of nAChR ligands, particularly because correlations have been traced between nicotinic cholinergic dysfunctions in the brain and the severity of certain symptoms of neurologic disorders such as Alzheimer's disease (AD), Parkinson's disease (PD), Down Syndrome (DS), schizophrenia, and some forms of epilepsy (Steinlein et al, 1995;Kuryatov et al, 1997;Hellstrom-Lindahl et al, 1999;Nordberg, 1999;Sihver et al, 1999;Perry et al, 1990Perry et al, , 2000Leonard et al, 2000;Court et al, 2001). A number of unconventional ligands that modulate nAChR activity have been discovered and, as a consequence of a continuum of basic and clinical research, the cholinesterase inhibitor galantamine, which also acts as a nicotinic allosteric potentiating ligand (APL), was recently approved by the Food and Drug Administration (FDA) for treatment of patients with AD in the United States.…”

Section: Introductionmentioning

confidence: 99%

Unconventional ligands and modulators of nicotinic receptors

et al. 2002

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ABSTRACT:Evidence gathered from epidemiologic and behavioral studies have indicated that neuronal nicotinic receptors (nAChRs) are intimately involved in the pathogenesis of a number of neurologic disorders, including Alzheimer's disease, Parkinson's disease, and schizophrenia. In the mammalian brain, neuronal nAChRs, in addition to mediating fast synaptic transmission, modulate fast synaptic transmission mediated by the major excitatory and inhibitory neurotransmitters glutamate and GABA, respectively. Of major interest, however, is the fact that the activity of the different subtypes of neuronal nAChR is also subject to modulation by substances of endogenous origin such as choline, the tryptophan metabolite kynurenic acid, neurosteroids, and ␤-amyloid peptides and by exogenous substances, including the so-called nicotinic allosteric potentiating ligands, of which galantamine is the prototype, and psychotomimetic drugs such as phencyclidine and ketamine. The present article reviews and discusses the effects of unconventional ligands on nAChR activity and briefly describes the potential benefits of using some of these compounds in the treatment of neuropathologic conditions in which nAChR function/expression is known to be altered.

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Nicotinic receptor abnormalities in Alzheimer’s disease

Cited by 209 publications

References 64 publications

Nicotinic Acetylcholine Receptor Distribution in Alzheimer's Disease, Dementia with Lewy Bodies, Parkinson's Disease, and Vascular Dementia: In Vitro Binding Study Using 5-[125I]-A-85380

Nicotinic Acetylcholine Receptor Distribution in Alzheimer's Disease, Dementia with Lewy Bodies, Parkinson's Disease, and Vascular Dementia: In Vitro Binding Study Using 5-[125I]-A-85380

Choline reverses scopolamine-induced memory impairment by improving memory reconsolidation

Unconventional ligands and modulators of nicotinic receptors

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