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1.
Introduction
Lifetime risks are the probabilities of progressing to Alzheimer's disease (AD) dementia during one's lifespan. Here, we report the first estimates of the lifetime and ten-year risks of AD dementia based on age, gender, and biomarker tests for preclinical disease.Methods
We used a multistate model for the disease process together with US death rates.Results
Lifetime risks of AD dementia vary considerably by age, gender, and the preclinical or clinical disease state of the individual. For example, the lifetime risks for a female with only amyloidosis are 8.4% for a 90-year old and 29.3% for a 65-year old. Persons younger than 85 years with mild cognitive impairment, amyloidosis, and neurodegeneration have lifetime risks of AD dementia greater than 50%.Discussion
Most persons with preclinical AD will not develop AD dementia during their lifetimes. Lifetime risks help interpret the clinical significance of biomarker screening tests for AD. 相似文献2.
Jordi Pegueroles Eduard Vilaplana Victor Montal Frederic Sampedro Daniel Alcolea Maria Carmona-Iragui Jordi Clarimon Rafael Blesa Alberto Lleó Juan Fortea 《Alzheimer's & dementia》2017,13(5):499-509
Introduction
Brain structural changes in preclinical Alzheimer's disease (AD) are poorly understood.Methods
We compared the changes in cortical thickness in the ADNI cohort during a 2-year follow-up between the NIA-AA preclinical AD stages defined by cerebrospinal fluid (CSF) biomarker levels. We also analyzed the correlation between baseline CSF biomarkers and cortical atrophy rates.Results
At follow-up, stage 1 subjects showed reduced atrophy rates in medial frontal areas and precuneus compared to stage 0 subjects, whereas stage 2/3 subjects presented accelerated atrophy in medial temporal structures. Low CSF Aβ1–42 levels were associated with reduced atrophy rates in subjects with normal tau levels and high CSF tau levels with accelerated atrophy only in subjects with low Aβ1–42 levels.Discussion
Our longitudinal data confirm a biphasic trajectory of changes in brain structure in preclinical AD. These have implications in AD trials, both in patient selection and the use of MRI as a surrogate marker of efficacy. 相似文献3.
Andrea Vergallo René-Sosata Bun Nicola Toschi Filippo Baldacci Henrik Zetterberg Kaj Blennow Enrica Cavedo Foudil Lamari Marie-Odile Habert Bruno Dubois Roberto Floris Francesco Garaci Simone Lista Harald Hampel 《Alzheimer's & dementia》2018,14(12):1623-1631
Introduction
Several neurodegenerative brain proteinopathies, including Alzheimer's disease (AD), are associated with cerebral deposition of insoluble aggregates of α-synuclein. Previous studies reported a trend toward increased cerebrospinal fluid (CSF) α-synuclein (α-syn) concentrations in AD compared with other neurodegenerative diseases and healthy controls.Methods
The pathophysiological role of CSF α-syn in asymptomatic subjects at risk of AD has not been explored. We performed a large-scale cross-sectional observational monocentric study of preclinical individuals at risk for AD (INSIGHT-preAD).Results
We found a positive association between CSF α-syn concentrations and brain β-amyloid deposition measures as mean cortical standard uptake value ratios. We demonstrate positive correlations between CSF α-syn and both CSF t-tau and p-tau181 concentrations.Discussion
Animal models presented evidence, indicating that α-syn may synergistically and directly induce fibrillization of both tau and β-amyloid. Our data indicate an association of CSF α-syn with AD-related pathophysiological mechanisms, during the preclinical phase of the disease. 相似文献4.
Ron Brookmeyer Nada Abdalla Claudia H. Kawas María M. Corrada 《Alzheimer's & dementia》2018,14(2):121-129
Introduction
We forecast the prevalence of preclinical and clinical Alzheimer's disease (AD) and evaluated potential impacts of primary and secondary preventions in the United States.Methods
We used a multistate model incorporating biomarkers for preclinical AD with US population projections.Results
Approximately 6.08 million Americans had either clinical AD or mild cognitive impairment due to AD in 2017 and that will grow to 15.0 million by 2060. In 2017, 46.7 million Americans had preclinical AD (amyloidosis, neurodegeneration, or both), although many may not progress to clinical disease during their lifetimes. Primary and secondary preventions have differential impact on future disease burden.Discussion
Because large numbers of persons are living with preclinical AD, our results underscore the need for secondary preventions for persons with existing AD brain pathology who are likely to develop clinical disease during their lifetimes as well as primary preventions for persons without preclinical disease. 相似文献5.
Tharick A. Pascoal Sulantha Mathotaarachchi Monica Shin Andrea L. Benedet Sara Mohades Seqian Wang Tom Beaudry Min Su Kang Jean-Paul Soucy Aurelie Labbe Serge Gauthier Pedro Rosa-Neto 《Alzheimer's & dementia》2017,13(6):644-653
Introduction
Recent literature proposes that amyloid β (Aβ) and phosphorylated tau (p-tau) synergism accelerates biomarker abnormalities in controls. Yet, it remains to be answered whether this synergism is the driving force behind Alzheimer disease (AD) dementia.Methods
We stratified 314 mild cognitive impairment individuals using [18F]florbetapir positron emission tomography Aβ imaging and cerebrospinal fluid p-tau. Regression and voxel-based logistic regression models with interaction terms evaluated 2-year changes in cognition and clinical status as a function of baseline biomarkers.Results
We found that the synergism between [18F]florbetapir and p-tau, rather than their additive effects, was associated with the cognitive decline and progression to AD. Furthermore, voxel-based analysis revealed that temporal and inferior parietal were the regions where the synergism determined an increased likelihood of developing AD.Discussion
Together, the present results support that progression to AD dementia is driven by the synergistic rather than a mere additive effect between Aβ and p-tau proteins. 相似文献6.
Marc Teichmann Stéphane Epelbaum Dalila Samri Marcel Levy Nogueira Agnès Michon Harald Hampel Foudil Lamari Bruno Dubois 《Alzheimer's & dementia》2017,13(8):913-923
Introduction
The International Working Group recommended the Free and Cued Selective Reminding Test (FCSRT) as a sensitive detector of the amnesic syndrome of the hippocampal type in typical Alzheimer's disease (AD). But does it differentiate AD from other neurodegenerative diseases?Methods
We assessed the FCSRT and cerebrospinal fluid (CSF) AD biomarkers in 992 cases. Experts, blinded to biomarker data, attributed in 650 cases a diagnosis of typical AD, frontotemporal dementia, posterior cortical atrophy, Lewy body disease, progressive supranuclear palsy, corticobasal syndrome, primary progressive aphasias, “subjective cognitive decline,” or depression.Results
The FCSRT distinguished typical AD from all other conditions with a sensitivity of 100% and a specificity of 75%. Non-AD neurodegenerative diseases with positive AD CSF biomarkers (“atypical AD”) did not have lower FCSRT scores than those with negative biomarkers.Discussion
The FCSRT is a reliable tool for diagnosing typical AD among various neurodegenerative diseases. At an individual level, however, its specificity is not absolute. Our findings also widen the spectrum of atypical AD to multiple neurodegenerative conditions. 相似文献7.
Ann D. Cohen Eric McDade Brad Christian Julie Price Chester Mathis William Klunk Benjamin L. Handen 《Alzheimer's & dementia》2018,14(6):743-750
Introduction
The objective of this study was to evaluate amyloid β (Aβ) deposition patterns in different groups of cerebral β amyloidosis: (1) nondemented with amyloid precursor protein overproduction (Down syndrome); (2) nondemented with abnormal processing of amyloid precursor protein (preclinical autosomal dominant Alzheimer disease); (3) presumed alteration in Aβ clearance with clinical symptoms (late-onset AD); and (4) presumed alterations in Aβ clearance (preclinical AD).Methods
We performed whole-brain voxelwise comparison of cerebral Aβ between 23 Down syndrome, 10 preclinical autosomal dominant Alzheimer disease, 17 late-onset AD, and 16 preclinical AD subjects, using Pittsburgh Compound B–positron emission tomography.Results
We found both Down syndrome and preclinical autosomal dominant Alzheimer disease shared a distinct pattern of increased bilateral striatal and thalamic Aβ deposition compared to late-onset AD and preclinical AD.Conclusion
Disorders associated with early-life alterations in amyloid precursor protein production or processing are associated with a distinct pattern of early striatal fibrillary Aβ deposition before significant cognitive impairment. A better understanding of this unique pattern could identify important mechanisms of Aβ deposition and possibly important targets for early intervention. 相似文献8.
Stephan Müller Oliver Preische Hamid R. Sohrabi Susanne Gräber Mathias Jucker John M. Ringman Ralph N. Martins Eric McDade Peter R. Schofield Bernardino Ghetti Martin Rossor Nick N. Fox Neill R. Graff-Radford Johannes Levin Adrian Danek Jonathan Vöglein Stephen Salloway Chengjie Xiong Christoph Laske 《Alzheimer's & dementia》2018,14(11):1427-1437
Introduction
Little is known about effects of physical activity (PA) in genetically driven early-onset autosomal dominant Alzheimer's disease (AD).Methods
A total of 372 individuals participating at the Dominantly Inherited Alzheimer Network study were examined to evaluate the cross-sectional relationship of PA with cognitive performance, functional status, cognitive decline, and AD biomarkers in cerebrospinal fluid. Mutation carriers were categorized as high or low exercisers according to WHO recommendations.Results
Mutation carriers with high PA showed significantly better cognitive and functional performance and significantly less AD-like pathology in cerebrospinal fluid than individuals with low PA. Mutation carriers with high PA scored 3.4 points better on Mini Mental State Examination at expected symptom onset and fulfilled the diagnosis of very mild dementia 15.1 years later compared with low exercisers.Discussion
These results support a beneficial effect of PA on cognition and AD pathology even in individuals with genetically driven autosomal dominant AD. 相似文献9.
Michael W. Weiner Dallas P. Veitch Paul S. Aisen Laurel A. Beckett Nigel J. Cairns Robert C. Green Danielle Harvey Clifford R. Jack William Jagust John C. Morris Ronald C. Petersen Jennifer Salazar Andrew J. Saykin Leslie M. Shaw Arthur W. Toga John Q. Trojanowski 《Alzheimer's & dementia》2017,13(5):561-571
Introduction
The overall goal of the Alzheimer's Disease Neuroimaging Initiative (ADNI) is to validate biomarkers for Alzheimer's disease (AD) clinical trials. ADNI-3, which began on August 1, 2016, is a 5-year renewal of the current ADNI-2 study.Methods
ADNI-3 will follow current and additional subjects with normal cognition, mild cognitive impairment, and AD using innovative technologies such as tau imaging, magnetic resonance imaging sequences for connectivity analyses, and a highly automated immunoassay platform and mass spectroscopy approach for cerebrospinal fluid biomarker analysis. A Systems Biology/pathway approach will be used to identify genetic factors for subject selection/enrichment. Amyloid positron emission tomography scanning will be standardized using the Centiloid method. The Brain Health Registry will help recruit subjects and monitor subject cognition.Results
Multimodal analyses will provide insight into AD pathophysiology and disease progression.Discussion
ADNI-3 will aim to inform AD treatment trials and facilitate development of AD disease-modifying treatments. 相似文献10.
Carly Oboudiyat Tamar Gefen Eleni Varelas Sandra Weintraub Emily Rogalski Eileen H. Bigio M.-Marsel Mesulam 《Alzheimer's & dementia》2017,13(5):598-601
Introduction
The accuracy of cerebrospinal fluid (CSF) biomarkers for detecting Alzheimer's disease (AD) pathology has not been fully validated in autopsied nonamnestic dementias.Methods
We retrospectively evaluated CSF amyloid β 1–42, phosphorylated-tau, and amyloid-tau index as predictors of Alzheimer pathology in patients with primary progressive aphasia, frontotemporal dementia, and progressive supranuclear palsy.Results
Nineteen nonamnestic autopsied cases with relevant CSF values were included. At autopsy, nine had AD and 10 had non-AD pathologies. All six patients whose combined CSF phosphorylated-tau and amyloid β levels were “consistent with AD” had postmortem Alzheimer pathology. The two patients whose biomarker values were “not consistent with AD” had non-AD pathologies. The CSF values of the remaining eight non-AD cases were in conflicting or borderline ranges.Discussion
CSF biomarkers reliably identified Alzheimer pathology in nonamnestic dementias and may be useful as a screening measure for inclusion of nonamnestic cases into Alzheimer's trials. 相似文献11.
Auriel A. Willette Joseph L. Webb Michael W. Lutz Barbara B. Bendlin Alexandra M. Wennberg Jennifer M. Oh Allen Roses Rebecca L. Koscik Bruce P. Hermann N. Maritza Dowling Sanjay Asthana Sterling C. Johnson 《Alzheimer's & dementia》2017,13(11):1217-1225
Introduction
Family history (FH) of Alzheimer's disease (AD) affects mitochondrial function and may modulate effects of translocase of the outer mitochondrial membrane 40 kDa (TOMM40) rs10524523 (‘523) poly-T length on memory decline.Methods
For 912 nonapolipoprotein ε4 middle-aged adults and 365 aged adults across the AD spectrum, linear mixed models gauged FH and TOMM40 ‘523 interactions on memory and global cognition between baseline and up to 10 years later. A cerebrospinal fluid mitochondrial function biomarker was also assessed.Results
For FH negative participants, gene-dose preservation of memory and global cognition was seen for “very long” versus “short” carriers. For FH positive, an opposite gene-dose decline was seen for very long versus short carriers. Maternal FH was a stronger predictor in aged, but not middle-aged, participants. Similar gene-dose effects were seen for the mitochondrial biomarker aspartate aminotransferase.Discussion
These results may clarify conflicting findings on TOMM40 poly-T length and AD-related decline. 相似文献12.
Min Shi Lu Tang Jon B. Toledo Carmen Ginghina Hua Wang Patrick Aro Poul H. Jensen Daniel Weintraub Alice S. Chen-Plotkin David J. Irwin Murray Grossman Leo McCluskey Lauren B. Elman David A. Wolk Edward B. Lee Leslie M. Shaw John Q. Trojanowski Jing Zhang 《Alzheimer's & dementia》2018,14(8):1052-1062
Introduction
The ability of Alzheimer's disease (AD) cerebrospinal fluid (CSF) biomarkers (amyloid β peptide 1–42, total tau, and phosphorylated tau) to discriminate AD from related disorders is limited. Biomarkers for other concomitant pathologies (e.g., CSF α-synuclein [α-syn] for Lewy body pathology) may be needed to further improve the differential diagnosis.Methods
CSF total α-syn, phosphorylated α-syn at Ser129, and AD CSF biomarkers were evaluated with Luminex immunoassays in 367 participants, followed by validation in 74 different neuropathologically confirmed cases.Results
CSF total α-syn, when combined with amyloid β peptide 1–42 and either total tau or phosphorylated tau, improved the differential diagnosis of AD versus frontotemporal dementia, Lewy body disorders, or other neurological disorders. The diagnostic accuracy of the combined models attained clinical relevance (area under curve ～0.9) and was largely validated in neuropathologically confirmed cases.Discussion
Combining CSF biomarkers representing AD and Lewy body pathologies may have clinical value in the differential diagnosis of AD. 相似文献13.
Background
TMS is safe and effective in the treatment of MDD, but as with other treatments, relapse may occur on cessation of treatment.Objective
To prevent relapse in MDD, following successful acute TMS treatment.Method
5 TMS treatments over 3 days, repeated at about monthly intervals.Results
14 patients received this care for more than 12 months. At the commencement of each series the mood scores were close to relapse, but at completion they were in the remitted range.Conclusion
Such treatment is useful. It is better conceptualized as relapse prevention rather than remittance maintenance. 相似文献14.
Jon B. Toledo Matthias Arnold Gabi Kastenmüller Rui Chang Rebecca A. Baillie Xianlin Han Madhav Thambisetty Jessica D. Tenenbaum Karsten Suhre J. Will Thompson Lisa St. John-Williams Siamak MahmoudianDehkordi Daniel M. Rotroff John R. Jack Alison Motsinger-Reif Shannon L. Risacher Colette Blach Joseph E. Lucas Rima Kaddurah-Daouk 《Alzheimer's & dementia》2017,13(9):965-984
Introduction
The Alzheimer's Disease Research Summits of 2012 and 2015 incorporated experts from academia, industry, and nonprofit organizations to develop new research directions to transform our understanding of Alzheimer's disease (AD) and propel the development of critically needed therapies. In response to their recommendations, big data at multiple levels are being generated and integrated to study network failures in disease. We used metabolomics as a global biochemical approach to identify peripheral metabolic changes in AD patients and correlate them to cerebrospinal fluid pathology markers, imaging features, and cognitive performance.Methods
Fasting serum samples from the Alzheimer's Disease Neuroimaging Initiative (199 control, 356 mild cognitive impairment, and 175 AD participants) were analyzed using the AbsoluteIDQ-p180 kit. Performance was validated in blinded replicates, and values were medication adjusted.Results
Multivariable-adjusted analyses showed that sphingomyelins and ether-containing phosphatidylcholines were altered in preclinical biomarker-defined AD stages, whereas acylcarnitines and several amines, including the branched-chain amino acid valine and α-aminoadipic acid, changed in symptomatic stages. Several of the analytes showed consistent associations in the Rotterdam, Erasmus Rucphen Family, and Indiana Memory and Aging Studies. Partial correlation networks constructed for Aβ1–42, tau, imaging, and cognitive changes provided initial biochemical insights for disease-related processes. Coexpression networks interconnected key metabolic effectors of disease.Discussion
Metabolomics identified key disease-related metabolic changes and disease-progression-related changes. Defining metabolic changes during AD disease trajectory and its relationship to clinical phenotypes provides a powerful roadmap for drug and biomarker discovery. 相似文献15.
Panos Theofilas Alexander J. Ehrenberg Sara Dunlop Ana T. Di Lorenzo Alho Austin Nguy Renata Elaine Paraizo Leite Roberta Diehl Rodriguez Maria B. Mejia Claudia K. Suemoto Renata Eloah De Lucena Ferretti-Rebustini Livia Polichiso Camila F. Nascimento William W. Seeley Ricardo Nitrini Carlos Augusto Pasqualucci Wilson Jacob Filho Udo Rueb John Neuhaus Lea T. Grinberg 《Alzheimer's & dementia》2017,13(3):236-246
Introduction
Alzheimer's disease (AD) progression follows a specific spreading pattern, emphasizing the need to characterize those brain areas that degenerate first. The brainstem's locus coeruleus (LC) is the first area to develop neurofibrillary changes (neurofibrillary tangles [NFTs]).Methods
The methods include unbiased stereological analyses in human brainstems to estimate LC volume and neuronal population in controls and individuals across all AD stages.Results
As the Braak stage increases by 1 unit, the LC volume decreases by 8.4%. Neuronal loss started only midway through AD progression. Age-related changes spare the LC.Discussion
The long gap between NFT accumulation and neuronal loss suggests that a second trigger may be necessary to induce neuronal death in AD. Imaging studies should determine whether LC volumetry can replicate the stage-wise atrophy observed here and how these changes are specific to AD. LC volumetry may develop into a screening biomarker for selecting high-yield candidates to undergo expensive and less accessible positron emission tomography scans and to monitor AD progression from presymptomatic stages. 相似文献16.
Belinda M. Brown Hamid R. Sohrabi Kevin Taddei Samantha L. Gardener Stephanie R. Rainey-Smith Jeremiah J. Peiffer Chengjie Xiong Anne M. Fagan Tammie Benzinger Virginia Buckles Kirk I. Erickson Roger Clarnette Tejal Shah Colin L. Masters Michael Weiner Nigel Cairns Martin Rossor Neill R. Graff-Radford Ralph N. Martins 《Alzheimer's & dementia》2017,13(11):1197-1206
Introduction
The objective of this study was to evaluate the relationship between self-reported exercise levels and Alzheimer's disease (AD) biomarkers, in a cohort of autosomal dominant AD mutation carriers.Methods
In 139 presymptomatic mutation carriers from the Dominantly Inherited Alzheimer Network, the relationship between self-reported exercise levels and brain amyloid load, cerebrospinal fluid (CSF) Aβ42, and CSF tau levels was evaluated using linear regression.Results
No differences in brain amyloid load, CSF Aβ42, or CSF tau were observed between low and high exercise groups. Nevertheless, when examining only those already accumulating AD pathology (i.e., amyloid positive), low exercisers had higher mean levels of brain amyloid than high exercisers. Furthermore, the interaction between exercise and estimated years from expected symptom onset was a significant predictor of brain amyloid levels.Discussion
Our findings indicate a relationship exists between self-reported exercise levels and brain amyloid in autosomal dominant AD mutation carriers. 相似文献17.
Stefan J. Teipel Enrica Cavedo Simone Lista Marie-Odile Habert Marie-Claude Potier Michel J. Grothe Stephane Epelbaum Luisa Sambati Geoffroy Gagliardi Nicola Toschi Michael D. Greicius Bruno Dubois Harald Hampel 《Alzheimer's & dementia》2018,14(9):1126-1136
Introduction
Cognitive change in people at risk of Alzheimer's disease (AD) such as subjective memory complainers is highly variable across individuals.Methods
We used latent class growth modeling to identify distinct classes of nonlinear trajectories of cognitive change over 2 years follow-up from 265 subjective memory complainers individuals (age 70 years and older) of the INSIGHT-preAD cohort. We determined the effect of cortical amyloid load, hippocampus and basal forebrain volumes, and education on the cognitive trajectory classes.Results
Latent class growth modeling identified distinct nonlinear cognitive trajectories. Education was associated with higher performing trajectories, whereas global amyloid load and basal forebrain atrophy were associated with lower performing trajectories.Discussion
Distinct classes of cognitive trajectories were associated with risk and protective factors of AD. These associations support the notion that the identified cognitive trajectories reflect different risk for AD that may be useful for selecting high-risk individuals for intervention trials. 相似文献18.
Takeshi Iwatsubo Atsushi Iwata Kazushi Suzuki Ryoko Ihara Hiroyuki Arai Kenji Ishii Michio Senda Kengo Ito Takeshi Ikeuchi Ryozo Kuwano Hiroshi Matsuda Chung-Kai Sun Laurel A. Beckett Ronald C. Petersen Michael W. Weiner Paul S. Aisen Michael C. Donohue 《Alzheimer's & dementia》2018,14(8):1077-1087
Introduction
We conducted Japanese Alzheimer's Disease Neuroimaging Initiative (J-ADNI) and compared the basic characteristics and progression profiles with those of ADNI in North America.Methods
A total of 537 Japanese subjects with normal cognition, late amnestic mild cognitive impairment (LMCI), or mild Alzheimer's disease (AD) were enrolled using the same criteria as ADNI. Rates of changes in representative cognitive or functional measures were compared for amyloid positron emission tomography- or cerebrospinal fluid amyloid β(1–42)-positive LMCI and mild AD between J-ADNI and ADNI.Results
Amyloid positivity rates were significantly higher in normal cognition of ADNI but at similar levels in LMCI and mild AD between J-ADNI and ADNI. Profiles of decline in cognitive or functional measures in amyloid-positive LMCI in J-ADNI (n = 75) and ADNI (n = 269) were remarkably similar, whereas those in mild AD were milder in J-ADNI (n = 73) compared with ADNI (n = 230).Discussion
These results support the feasibility of bridging of clinical trials in the prodromal stage of AD between Asia and western countries. 相似文献19.
Paolo Bosco Alberto Redolfi Martina Bocchetta Clarissa Ferrari Anna Mega Samantha Galluzzi Mark Austin Andrea Chincarini D. Louis Collins Simon Duchesne Bénédicte Maréchal Alexis Roche Francesco Sensi Robin Wolz Montserrat Alegret Frederic Assal Mircea Balasa Christine Bastin Giovanni B. Frisoni 《Alzheimer's & dementia》2017,13(9):1013-1023
Introduction
Hippocampal volume is a core biomarker of Alzheimer's disease (AD). However, its contribution over the standard diagnostic workup is unclear.Methods
Three hundred fifty-six patients, under clinical evaluation for cognitive impairment, with suspected AD and Mini–Mental State Examination ≥20, were recruited across 17 European memory clinics. After the traditional diagnostic workup, diagnostic confidence of AD pathology (DCAD) was estimated by the physicians in charge. The latter were provided with the results of automated hippocampal volumetry in standardized format and DCAD was reassessed.Results
An increment of one interquartile range in hippocampal volume was associated with a mean change of DCAD of ?8.0% (95% credible interval: [?11.5, ?5.0]). Automated hippocampal volumetry showed a statistically significant impact on DCAD beyond the contributions of neuropsychology, 18F-fluorodeoxyglucose positron emission tomography/single-photon emission computed tomography, and cerebrospinal fluid markers (?8.5, CrI: [?11.5, ?5.6]; ?14.1, CrI: [?19.3, ?8.8]; ?10.6, CrI: [?14.6, ?6.1], respectively).Discussion
There is a measurable effect of hippocampal volume on DCAD even when used on top of the traditional diagnostic workup. 相似文献20.
Despite increasing attention to the application of transcranial Direct Current Stimulation (tDCS) for enhancing cognitive functions in subjects exposing to varying degree of cerebral atrophy such as Alzheimer's disease (AD), aging, and mild cognitive impairment (MCI), there is no general information for customizing stimulation protocol.