Motor cortex excitability in Alzheimer disease: one year follow-up study

Pennisi, Giovanni; Alagona, Giovanna; Ferri, Raffaele; Greco, Salvatore; Santonocito, D.; Pappalardo, A; Bella, Rita

doi:10.1016/s0304-3940(02)00701-2

Cited by 79 publications

(44 citation statements)

References 14 publications

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“…This possible explanation is in line with previous evidence of abnormal central EEG rhythms or evoked potentials in AD subjects performing voluntary movements or perceiving somatosensory stimuli (Babiloni et al, 2000;Ferri et al, 1996). Furthermore, abnormally hyperexcitable primary motor cortex has been recently reported in AD, as revealed by EEG rhythms related to self-paced movements and transcranial magnetic stimulation (Babiloni et al, 2000;Pennisi et al, 2002;Ferreri et al, 2003;).…”

Section: Relative Power and Frequency Of Alpha Rhythms In Mild Dementiasupporting

confidence: 89%

Individual analysis of EEG frequency and band power in mild Alzheimer's disease

Moretti

Babiloni

Binetti

et al. 2004

Clinical Neurophysiology

337

251

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Objective: This EEG study investigates the role of the cholinergic system, cortico-cortical connections, and sub-cortical white matter on the relationship between individual EEG frequencies and their relative power bands.Methods: EEGs were recorded at rest in 30 normal elderly subjects (Nold), 60 mild Alzheimer disease (AD) and 20 vascular dementia (VaD) patients, comparable for Mini Mental State Evaluation scores . Individual EEG frequencies were indexed by the theta/alpha transition frequency (TF) and by the individual alpha frequency (IAF) with power peak in the extended alpha range (5 -14 Hz). Relative power was separately computed for delta, theta, alpha1, alpha2, and alpha3 bands, on the basis of the TF and IAF.Results: Using normal subjects as a reference, VaD patients showed 'slowing' of alpha frequency (TF-IAF) and lower alpha2 power; Mild AD patients showed lower alpha2 and alpha3 power; delta power was higher in both AD and VaD patients; Theta power was higher only in VaD patients.Conclusions: Individual analysis of the alpha frequency and power can discriminate mild AD from VaD and normal elderly subjects.Significance: This analysis may probe pathophysiological mechanisms causing AD and VaD.

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Section: Relative Power and Frequency Of Alpha Rhythms In Mild Dementiasupporting

confidence: 89%

Individual analysis of EEG frequency and band power in mild Alzheimer's disease

Moretti

Babiloni

Binetti

et al. 2004

Clinical Neurophysiology

337

251

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“…These findings in AD patients confirm and support the previous reports [1,11,15,17]. The hyperexcitability is not due to aging, and in fact it has been shown as an increment of MT in elderly adults when compared with young subjects [14,20].…”

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confidence: 91%

Section: Introductionmentioning

confidence: 99%

“…It represents a valid tool to study the motor cortex excitability through the evaluation of the motor threshold (MT). In the last years, MT has been investigated in AD patients [1,15,17] but there are no reports available on motor cortex excitability in VaD patients.In the present work, motor cortex excitability changes were studied in AD and SIVD patients to assess the electrophysiological differentiation and the eventual usefulness of MT for a better clinical evaluation of these two types of dementia.Twenty SIVD patients (eight men, 12 women, age range 48-84 years, mean age 71.8^9.37 years), 20 AD patients (seven men, 13 women, age range 55-82 years, mean age 72.2^7.53 years) and 20 neurologically and cognitively intact subjects (eight men and 12 women, age range 52-80 years, mean age 68.55^7.96 years) were studied. The study was approved by the local ethics committee and informed consent was obtained from all patients (or from close relatives) and control subjects.…”

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confidence: 99%

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Motor cortex excitability in Alzheimer's disease and in subcortical ischemic vascular dementia

Alagona

Ferri

Pennisi

et al. 2004

Neuroscience Letters

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Twenty Alzheimer's disease (AD) patients, 20 subcortical ischemic vascular dementia (SIVD) patients and 20 neurologically and cognitively normal subjects underwent transcranial magnetic stimulation to study motor cortex excitability changes. Motor threshold (MT), amplitude of motor evoked potentials, silent period and the H/M ratio (amplitude of maximal Hoffman reflex vs. that of maximal motor response) were considered. MT was lower in SIVD patients when compared with AD patients (P ¼ 0:003) and the control group (P , 0:001) and lower in AD patients when compared with the control group (P , 0:001). The increment of motor cortex excitability in AD and SIVD did not lead us to distinguish clearly the two types of dementia. It is likely that the electrophysiological similarity between AD and SIVD could represent another common mechanism shared from these forms of dementia. q 2004 Elsevier Ireland Ltd. All rights reserved.Keywords: Alzheimer's disease; Subcortical ischemic vascular dementia; Motor cortex excitability; Transcranial magnetic stimulation Alzheimer's disease (AD) and vascular dementia (VaD) are the two most common forms of dementia, which share many pathological, symptomatic and neurochemical features [10]. Subcortical ischemic vascular dementia (SIVD) represents an important and homogeneous subtype of VaD [5]. Transcranial magnetic stimulation (TMS) is the method of choice for noninvasive stimulation of human brain in conscious subjects. It represents a valid tool to study the motor cortex excitability through the evaluation of the motor threshold (MT). In the last years, MT has been investigated in AD patients [1,15,17] but there are no reports available on motor cortex excitability in VaD patients.In the present work, motor cortex excitability changes were studied in AD and SIVD patients to assess the electrophysiological differentiation and the eventual usefulness of MT for a better clinical evaluation of these two types of dementia.Twenty SIVD patients (eight men, 12 women, age range 48-84 years, mean age 71.8^9.37 years), 20 AD patients (seven men, 13 women, age range 55-82 years, mean age 72.2^7.53 years) and 20 neurologically and cognitively intact subjects (eight men and 12 women, age range 52-80 years, mean age 68.55^7.96 years) were studied. The study was approved by the local ethics committee and informed consent was obtained from all patients (or from close relatives) and control subjects. All patients and control subjects were free of acetylcholinesterase inhibitors or other medications able to induce cortical or spinal excitability changes. The diagnosis of probable SIVD was established on a modification [5] of the NINDS-AIREN

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“…However, it remains to be determined how those reductions affected the function of GABA A Rs in cellular membranes. This lack of information is a critical void, considering the correlation between cortical hyperexcitability, the pathological state of patients with AD (12,13), and the protective effects of GABA A R agonists against Aβ-induced injury (14). In the present study, we have extended our previous observations and report clear evidence of functional remodeling of native human GABA A Rs in AD.…”

supporting

confidence: 74%

Loss of functional GABA _A receptors in the Alzheimer diseased brain

Limón

Reyes-Ruiz

Miledi

2012

Proc. Natl. Acad. Sci. U.S.A.

236

176

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The cholinergic and glutamatergic neurotransmission systems are known to be severely disrupted in Alzheimer's disease (AD). GABAergic neurotransmission, in contrast, is generally thought to be well preserved. Evidence from animal models and human postmortem tissue suggest GABAergic remodeling in the AD brain. Nevertheless, there is no information on changes, if any, in the electrophysiological properties of human native GABA receptors as a consequence of AD. To gain such information, we have microtransplanted cell membranes, isolated from temporal cortices of control and AD brains, into Xenopus oocytes, and recorded the electrophysiological activity of the transplanted GABA receptors. We found an age-dependent reduction of GABA currents in the AD brain. This reduction was larger when the AD membranes were obtained from younger subjects. We also found that GABA currents from AD brains have a faster rate of desensitization than those from non-AD brains. Furthermore, GABA receptors from AD brains were slightly, but significantly, less sensitive to GABA than receptors from non-AD brains. The reduction of GABA currents in AD was associated with reductions of mRNA and protein of the principal GABA receptor subunits normally present in the temporal cortex. Pairwise analysis of the transcripts within control and AD groups and analyses of the proportion of GABA receptor subunits revealed down-regulation of α1 and γ2 subunits in AD. In contrast, the proportions of α2, β1, and γ1 transcripts were up-regulated in the AD brains. Our data support a functional remodeling of GABAergic neurotransmission in the human AD brain.neurodegeneration | synaptic mechanism | gephyrin | glutamate receptor A lzheimer's disease (AD) is associated with a widespread loss of synapse density and continuous degeneration of cholinergic and glutamatergic pathways (1). Although disruption of excitatory pathways is broadly accepted, inhibitory GABAergic pathways are generally thought to be well preserved in AD (reviewed in refs. 2, 3). GABA receptors (GABA A Rs) are pentameric complexes formed by combinations of α1-6, β1-3, γ1-2, and δ subunits; the specific combination or stoichiometry of the different GABA A R subunits contributes to their cellular localization, pharmacological profile, and function (4). Early studies of the temporal cortex, an area greatly affected by the neuropathic hallmarks of AD, showed only slight decreases (13-17%) of benzodiazepine binding (2, 5), suggesting a modest decrease of GABA A Rs in AD. However, unspecific binding of benzodiazepines to voltage-dependent anion channels (6) and to mitochondrial translocator proteins (7) that are increased in AD (8) confound the interpretation of results. Lower levels of GABA A Rsubunits α1, α2, α4, δ, and β2 mRNAs in the prefrontal cortex of AD brains (3) and of α1, α5, and β3 mRNAs in the AD hippocampus (2, 9) suggest that some receptors may have an altered functional profile in AD. Our initial experiments, evaluating the feasibility of recording the activity of native receptors fro...

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Motor cortex excitability in Alzheimer disease: one year follow-up study

Cited by 79 publications

References 14 publications

Individual analysis of EEG frequency and band power in mild Alzheimer's disease

Individual analysis of EEG frequency and band power in mild Alzheimer's disease

Motor cortex excitability in Alzheimer's disease and in subcortical ischemic vascular dementia

Loss of functional GABA _A receptors in the Alzheimer diseased brain

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Motor cortex excitability in Alzheimer disease: one year follow-up study

Cited by 79 publications

References 14 publications

Individual analysis of EEG frequency and band power in mild Alzheimer's disease

Individual analysis of EEG frequency and band power in mild Alzheimer's disease

Motor cortex excitability in Alzheimer's disease and in subcortical ischemic vascular dementia

Loss of functional GABA A receptors in the Alzheimer diseased brain

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Product

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Loss of functional GABA _A receptors in the Alzheimer diseased brain