Evidence map›Paper›PMID 31727363›Full record

ArticleNeurobiology of aging2020

EEG spectral power abnormalities and their relationship with cognitive dysfunction in patients with Alzheimer's disease and type 2 diabetes.

Christopher S Y Benwell, Paula Davila-Pérez, Peter J Fried, Richard N Jones, Thomas G Travison, Emiliano Santarnecchi, Alvaro Pascual-Leone, Mouhsin M Shafi

Abstract read
In one paragraph

Article in Neurobiology of aging, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
57citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

57 citing papers in PubMed, 1 synthesis or guideline pooled it.

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  19. Machine learning based on event-related oscillations of working memory differentiates between preclinical Alzheimer's disease and normal aging.Clinical neurophysiology : official journal of the International Federation of Clinical Neurophysiology · 2025
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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.

Christopher S Y BenwellBerenson-Allen Center for Noninvasive Brain Stimulation, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, MA, USA; Division of Cognitive Neurology, Department of Neurology, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, MA, USA; Division of Psychology, School of Social Sciences, University of Dundee, Dundee, UK. Electronic address: c.benwell@dundee.ac.uk.
Paula Davila-PérezBerenson-Allen Center for Noninvasive Brain Stimulation, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, MA, USA; Division of Cognitive Neurology, Department of Neurology, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, MA, USA; Neuroscience and Motor Control Group (NEUROcom), Institute for Biomedical Research (INIBIC), Universidade da Coruña, A Coruña, Spain.
Peter J FriedBerenson-Allen Center for Noninvasive Brain Stimulation, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, MA, USA; Division of Cognitive Neurology, Department of Neurology, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, MA, USA.
Richard N JonesDepartment of Psychiatry and Human Behavior, Warren Alpert Medical School, Brown University, Butler Hospital, Providence, RI, USA.
Thomas G TravisonHinda and Arthur Marcus Institute for Aging Research, Hebrew Senior Life, Boston, MA, USA.
Emiliano SantarnecchiBerenson-Allen Center for Noninvasive Brain Stimulation, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, MA, USA; Division of Cognitive Neurology, Department of Neurology, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, MA, USA.
Alvaro Pascual-LeoneBerenson-Allen Center for Noninvasive Brain Stimulation, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, MA, USA; Division of Cognitive Neurology, Department of Neurology, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, MA, USA; Hinda and Arthur Marcus Institute for Aging Research, Hebrew Senior Life, Boston, MA, USA; Institut Guttman, Universitat Autonoma de Barcelona, Badalona, Barcelona, Spain; Center for Memory Health, Hebrew Senior Life, Boston, MA, USA.
Mouhsin M ShafiBerenson-Allen Center for Noninvasive Brain Stimulation, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, MA, USA; Division of Cognitive Neurology, Department of Neurology, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, MA, USA; Comprehensive Epilepsy Center, Department of Neurology, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, MA, USA. Electronic address: mshafi@bidmc.harvard.edu.

Funding

HARVARD CLINICAL AND TRANSLATIONAL SCIENCE CENTER (UL1)UL1RR025758 · NCRR · HARVARD MEDICAL SCHOOL · PI NADLER, LEE MARSHALL · 2008 to 2011
$91.4M
The Role of Inflammation in the Pathophysiology of Delirium and its Associated Long-Term Cognitive DeclineP01AG031720 · NIA · HEBREW REHABILITATION CENTER FOR AGED · PI SHAFI, MOUHSIN · 2010 to 2022
$26.7M
Gamma Induction for Amyloid Clearance in Alzheimer’s DiseaseR01AG060981 · NIA · MASSACHUSETTS GENERAL HOSPITAL · PI SANTARNECCHI, EMILIANO · 2019 to 2023
$3.5M
Transcranial Direct Current Stimulation and Robotic Training in Chronic StrokeR01HD069776 · NICHD · WINIFRED MASTERSON BURKE MED RES INST · PI EDWARDS, DYLAN JAMES · 2012 to 2016
$3.2M
Repetitive TMS-induced modulation of cortical excitability in ADR01MH115949 · NIMH · BETH ISRAEL DEACONESS MEDICAL CENTER · PI SHAFI, MOUHSIN · 2018 to 2022
$3.2M
Treating hyperexcitability in Alzheimer’s disease with levetiracetam to improve brain function and cognitionR01AG060987 · NIA · BETH ISRAEL DEACONESS MEDICAL CENTER · PI SHAFI, MOUHSIN · 2019 to 2023
$3.0M
The Development and Human Translation of Temporal Interference Brain StimulationR01MH117063 · NIMH · BETH ISRAEL DEACONESS MEDICAL CENTER · PI PRESS, DANIEL Z. · 2018 to 2021
$2.8M
Cortical connectivity, physiology, and response to stimulation in human epilepsyR01NS073601 · NINDS · BETH ISRAEL DEACONESS MEDICAL CENTER · PI CHANG, BERNARD S. · 2011 to 2015
$1.9M
Role of functional brain connectivity on efficacy of TMS for depressionR21MH099196 · NIMH · BETH ISRAEL DEACONESS MEDICAL CENTER · PI PASCUAL-LEONE, ALVARO · 2013 to 2014
$491k
Cortical plasticity in type II diabetes mellitusR21NS082870 · NINDS · BETH ISRAEL DEACONESS MEDICAL CENTER · PI PASCUAL-LEONE, ALVARO · 2013 to 2014
$490k
Transcranial Stimulation in Spino-Cerebellar AtaxiaR21NS085491 · NINDS · BETH ISRAEL DEACONESS MEDICAL CENTER · PI PASCUAL-LEONE, ALVARO · 2013 to 2014
$469k
NCRR NIH HHS UL1 RR025758NIA NIH HHS P01 AG031720NIA NIH HHS R01 AG060981NIA NIH HHS R01 AG060987NICHD NIH HHS R01 HD069776NIMH NIH HHS R01 MH115949NIMH NIH HHS R01 MH117063NIMH NIH HHS R21 MH099196NINDS NIH HHS R01 NS073601NINDS NIH HHS R21 NS082870NINDS NIH HHS R21 NS085491
6 · The paper itself

Abstract

Rhythmic neural activity has been proposed to play a fundamental role in cognition. Both healthy and pathological aging are characterized by frequency-specific changes in oscillatory activity. However, the cognitive relevance of these changes across the spectrum from normal to pathological aging remains unknown. We examined electroencephalography (EEG) correlates of cognitive function in healthy aging and 2 of the most prominent and debilitating age-related disorders: type 2 diabetes mellitus (T2DM) and Alzheimer's disease (AD). Relative to healthy controls (HC), patients with AD were impaired on nearly every cognitive measure, whereas patients with T2DM performed worse mainly on learning and memory tests. A continuum of alterations in resting-state EEG was associated with pathological aging, generally characterized by reduced alpha (α) and beta (β) power (AD < T2DM < HC) and increased delta (δ) and theta (θ) power (AD > T2DM > HC), with some variations across different brain regions. There were also reductions in the frequency and power density of the posterior dominant rhythm in AD. The ratio of (α + β)/(δ + θ) was specifically associated with cognitive function in a domain- and diagnosis-specific manner. The results thus captured both similarities and differences in the pathophysiology of cerebral oscillations in T2DM and AD. Overall, pathological brain aging is marked by a shift in oscillatory power from higher to lower frequencies, which can be captured by a single cognitively relevant measure of the ratio of (α + β) over (δ + θ) power.

Indexed as

Alzheimer DiseaseDiabetes Mellitus, Type 2ElectroencephalographyCognitive AgingCognitive DysfunctionAlzheimer's diseaseCognitive agingEEGNeuropsychologyOscillationsType-2 diabetes mellitus

Identifiers

PMID31727363
PMCPMC6942171

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Registered trials

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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.