Frontocerebellar gray matter plasticity in alcohol use disorder linked to abstinence

Müller, Angela; Meyerhoff, Dieter J.

doi:10.1016/j.nicl.2021.102788

Cited by 5 publications

(3 citation statements)

References 81 publications

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“…The SUD individuals were recruited from outpatient treatment clinics in San Francisco, CA, controls were recruited from the local community. Some of the T1 weighted data of this study have been used for two previous publications ( 30 , 31 ). PSU and AUD participants were ~1 month abstinent when scanned, OUD individuals were on maintenance medication when scanned.…”

Section: Methodsmentioning

confidence: 99%

Substance-Specific and Shared Gray Matter Signatures in Alcohol, Opioid, and Polysubstance Use Disorder

2022

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Substance use disorders (SUD) have been shown to be associated with gray matter (GM) loss, particularly in the frontal cortex. However, unclear is to what degree these regional GM alterations are substance-specific or shared across different substances, and if these regional GM alterations are independent of each other or the result of system-level processes at the intrinsic connectivity network level. The T1 weighted MRI data of 65 treated patients with alcohol use disorder (AUD), 27 patients with opioid use disorder (OUD) on maintenance therapy, 21 treated patients with stimulant use disorder comorbid with alcohol use disorder (polysubstance use disorder patients, PSU), and 21 healthy controls were examined via data-driven vertex-wise and voxel-wise GM analyses. Then, structural covariance analyses and open-access fMRI database analyses were used to map the cortical thinning patterns found in the three SUD groups onto intrinsic functional systems. Among AUD and OUD, we identified both common cortical thinning in right anterior brain regions as well as SUD-specific regional GM alterations that were not present in the PSU group. Furthermore, AUD patients had not only the most extended regional thinning but also significantly smaller subcortical structures and cerebellum relative to controls, OUD and PSU individuals. The system-level analyses revealed that AUD and OUD showed cortical thinning in several functional systems. In the AUD group the default mode network was clearly most affected, followed by the salience and executive control networks, whereas the salience and somatomotor network were highlighted as critical for understanding OUD. Structural brain alterations in groups with different SUDs are largely unique in their spatial extent and functional network correlates.

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Section: Methodsmentioning

confidence: 99%

Substance-Specific and Shared Gray Matter Signatures in Alcohol, Opioid, and Polysubstance Use Disorder

2022

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“…[219][220][221][222] Cross-sectional neuroimaging reports support AUD-related volume shrinkage in specific brain structures, including frontal, temporal, and parietal cortices; diencephalon; brain stem; and cerebellum. [223][224][225][226][227][228][229] In contrast to results of postmortem analyses of neuronal numbers, neuroimaging studies describe significant volume deficits in people with AUD, relative to healthy controls, in hippocampus and basal ganglia (i.e., caudate, putamen, nucleus accumbens) that may be accounted for by white matter compromise. 224,[230][231][232][233][234][235] Longitudinal studies that compare individuals with older age at AUD onset and relatively less lifetime alcohol use with individuals with younger age at AUD onset further support accelerated brain aging in frontal cortical volumes due to age-alcohol interactions and not just attributable to more years of alcohol misuse.…”

Section: Postmortem Neuropathologymentioning

confidence: 99%

“…227,[236][237][238][239] Other longitudinal studies show that alcohol abstinence is associated with brain integrity improvement (i.e., volume recovery), whereas relapse precipitates further volume shrinkage. [240][241][242][243][244] Individuals with AUD who relapse show continuing volume decline compared with those who achieve abstinence, 225,241,245,246 but even reduced drinking without achieving or maintaining complete abstinence can improve brain structure and function. 247 Similarly, a controlled longitudinal study that assessed individuals with AUD soon after withdrawal and then again after 2 weeks of sobriety suggested resolution of volume deficits specifically in hippocampal subfield CA2+3 248 (also see Zahr et al, 2019 232 ; Lee et al, 2016 249 ).…”

Section: Postmortem Neuropathologymentioning

confidence: 99%

Alcohol Use Disorder and Dementia: A Review

Zahr

2024

ARCR

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PURPOSE By 2040, 21.6% of Americans will be over age 65, and the population of those older than age 85 is estimated to reach 14.4 million. Although not causative, older age is a risk factor for dementia: every 5 years beyond age 65, the risk doubles; approximately one-third of those older than age 85 are diagnosed with dementia. As current alcohol consumption among older adults is significantly higher compared to previous generations, a pressing question is whether drinking alcohol increases the risk for Alzheimer’s disease or other forms of dementia. SEARCH METHODS Databases explored included PubMed, Web of Science, and ScienceDirect. To accomplish this narrative review on the effects of alcohol consumption on dementia risk, the literature covered included clinical diagnoses, epidemiology, neuropsychology, postmortem pathology, neuroimaging and other biomarkers, and translational studies. Searches conducted between January 12 and August 1, 2023, included the following terms and combinations: “aging,” “alcoholism,” “alcohol use disorder (AUD),” “brain,” “CNS,” “dementia,” “Wernicke,” “Korsakoff,” “Alzheimer,” “vascular,” “frontotemporal,” “Lewy body,” “clinical,” “diagnosis,” “epidemiology,” “pathology,” “autopsy,” “postmortem,” “histology,” “cognitive,” “motor,” “neuropsychological,” “magnetic resonance,” “imaging,” “PET,” “ligand,” “degeneration,” “atrophy,” “translational,” “rodent,” “rat,” “mouse,” “model,” “amyloid,” “neurofibrillary tangles,” “α-synuclein,” or “presenilin.” When relevant, “species” (i.e., “humans” or “other animals”) was selected as an additional filter. Review articles were avoided when possible. SEARCH RESULTS The two terms “alcoholism” and “aging” retrieved about 1,350 papers; adding phrases—for example, “postmortem” or “magnetic resonance”—limited the number to fewer than 100 papers. Using the traditional term, “alcoholism” with “dementia” resulted in 876 citations, but using the currently accepted term “alcohol use disorder (AUD)” with “dementia” produced only 87 papers. Similarly, whereas the terms “Alzheimer’s” and “alcoholism” yielded 318 results, “Alzheimer’s” and “alcohol use disorder (AUD)” returned only 40 citations. As pertinent postmortem pathology papers were published in the 1950s and recent animal models of Alzheimer’s disease were created in the early 2000s, articles referenced span the years 1957 to 2024. In total, more than 5,000 articles were considered; about 400 are herein referenced. DISCUSSION AND CONCLUSIONS Chronic alcohol misuse accelerates brain aging and contributes to cognitive impairments, including those in the mnemonic domain. The consensus among studies from multiple disciplines, however, is that alcohol misuse can increase the risk for dementia, but not necessarily Alzheimer’s disease. Key issues to consider include the reversibility of brain damage following abstinence from chronic alcohol misuse compared to the degenerative and progressive course of ...

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Cortical thickness of the inferior parietal lobule as a potential predictor of relapse in men with alcohol dependence

Yang,

Du,

Yang

et al. 2023

Brain Imaging and Behavior

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BackgroundAlcohol dependence (AD) is a disorder with a high recurrence rate that leads to a considerable public health burden. The risk of relapse appears to be related to a complex interplay of multiple factors. Herein, we aimed to explore the potential neural predictors of relapse in Chinese male patients with AD. MethodsThis study enrolled 58 male patients with AD who had undergone acute detoxi cation. General demographic information and clinical features were collected. Magnetic resonance imaging (MRI) data were used to measure cortical thickness across 34 regions of the brain. Patients were followed up at 6 months, and 51 patients completed the follow-up visit. These patients were divided into a relapser and an abstainer group. A binary logistic regression analysis was performed to investigate the potential risk factors of relapse. ResultsCompared to abstainers, relapsers showed higher inattention and non-planning impulsivity on the 11th version of the Barratt Impulsive Scale. The cortical thicknesses of the inferior-parietal lobule were signi cantly greater in abstainers compared with those in relapsers. Furthermore, binary logistic regression analysis showed that the thickness of the inferior parietal lobule predicted relapse. ConclusionsRelapsers show poorer impulse control than abstainers, and MRI imaging shows a decreased thickness of the inferior parietal lobule in relapsers. Our results indicate the thickness of the inferior parietal lobule as a potential relapse predictor in male patients with AD.

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Frontocerebellar gray matter plasticity in alcohol use disorder linked to abstinence

Abstract: Highlights GM loss in frontocerebellar circuit predicts relapse. GM recovery in AUD involves distinct neural processes. Recovery is not a reversal of any AUD-related GM damage.

Cited by 5 publications

References 81 publications

Substance-Specific and Shared Gray Matter Signatures in Alcohol, Opioid, and Polysubstance Use Disorder

Substance-Specific and Shared Gray Matter Signatures in Alcohol, Opioid, and Polysubstance Use Disorder

Alcohol Use Disorder and Dementia: A Review

Cortical thickness of the inferior parietal lobule as a potential predictor of relapse in men with alcohol dependence

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