Evidence map›Paper›PMID 21207079›Full record

ReviewJournal of neural transmission (Vienna, Austria : 1996)2011

Transcranial magnetic stimulation in Alzheimer's disease: a neurophysiological marker of cortical hyperexcitability.

Giovanni Pennisi, Raffaele Ferri, Giuseppe Lanza, Mariagiovanna Cantone, Manuela Pennisi, Valentina Puglisi, Giulia Malaguarnera, Rita Bella

Abstract readReview
PubMed Publisher
In one paragraph

Review in Journal of neural transmission (Vienna, Austria : 1996), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed, 3 pooled it
6.0field-weighted citation impact, top 4% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

39 citing papers in PubMed, 3 syntheses or guidelines pooled it, 85 citations in OpenAlex.

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  9. The Amyloid Precursor Protein Modulates the Position and Length of the Axon Initial Segment.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors at 2 institutions in 1 country.

Giovanni PennisiDepartment of Neuroscience, University of Catania, Catania, Italy. pennigi@unict.it
Raffaele Ferri
Giuseppe Lanza
Mariagiovanna Cantone
Manuela Pennisi
Valentina Puglisi
Giulia Malaguarnera
Rita Bella
University of Catania · ITOasi Maria SS · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Recently, neuropathological studies have shown an important motor cortex involvement in Alzheimer's disease (AD), even in its early stages, despite the lack of clinically evident motor deficit. Transcranial magnetic stimulation (TMS) studies have demonstrated that cortical excitability is enhanced in AD patients. This cortical hyperexcitability is believed to be a compensatory mechanism to execute voluntary movements, despite the progressive impairment of associative cortical areas. At present, it is not clear if these motor cortex excitability changes might be the expression of an involvement of intracortical excitatory glutamatergic circuits or an impairment of inhibitory cholinergic and, to a lesser extent, gabaergic activity. Although the main hypothesis for the pathogenesis of AD remains the degeneration of the basal forebrain cholinergic neurons, the development of specific TMS protocols, such as the paired-pulse TMS and the study of the short-latency afferent inhibition, points out the role of other neurotransmitters, such as gamma-amino-butyric acid, glutamate and dopamine. The potential therapeutic effect of repetitive TMS in restoring or compensating damaged cognitive functions, might become a possible rehabilitation tool in AD patients. Based on different patterns of cortical excitability, TMS may be useful in discriminating between physiological brain aging, mild cognitive impairment, AD and other dementing disorders. The present review provides a perspective of these TMS techniques by further understanding the role of different neurotransmission pathways and plastic remodelling of neuronal networks in the pathogenesis of AD.

Indexed as

Alzheimer DiseaseBiomarkersBrain WavesCerebral CortexElectromagnetic FieldsHumansMembrane PotentialsMovementTranscranial Magnetic StimulationVolitionBiomarkers

Identifiers

PMID21207079
OpenAlexW2013545829

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.