Alzheimer's Disease Dementia Research Articles

Temporal trend and attributable risk factors of Alzheimer's disease and other dementias burden in China: Findings from the Global Burden of Disease Study 2021.

We examined the burden of Alzheimer's disease and other dementias (ADOD) and attributable factors at the national and provincial levels in China. Using the Global Burden of Diseases Study 2021, we estimated incidence, prevalence, mortality rate, disability-adjusted life years (DALYs), and the ratio of years lived with disability (YLD) to DALYs for ADOD in China. Estimated annual percentage changes (EAPCs) were used to quantify the temporal trends from 1990 to 2021. In 2021, China experienced the highest ADOD burden among Group of 20 member nations. The EAPCs for age-standardized rates for incidence, age-standardized rates for prevalence, and age-standardized mortality rate were 0.41 (uncertainty intervals [UIs] 0.34-0.49); 0.44 (UI: 0.36-0.52); and -0.19 (UI: -0.23 to -0.15), respectively. Between 1990 and 2021, the number of people with ADOD increased by 322.18% and DALYs associated with ADOD increased by 272.71%; most of these increases were explained by population aging. Considering the aging Chinese population, targeted strategies to prevent dementia are urgently needed. China experienced the highest dementia burden among Group of 20 member nations. High body mass index, high fasting plasma glucose, and smoking were major risk factors for Alzheimer's disease and other dementias (ADOD) burden. Since 1990, the incidence and prevalence of ADOD increased substantially in China. The mortality rate related to ADOD decreased consistently. Considering the aging Chinese population, targeted strategies are urgently needed.

Supporting Arab-American Families Living With Dementia: Testing a Culturally Adapted Program.

Limited access to support services due to language and cultural barriers often results in a belief that family alone is the only option during times of need among Arab Americans. We test whether participation in a culturally adapted version of the Alzheimer's Association "Living with Alzheimer's" educational program is associated with positive outcomes for Arab-American care partners (N = 58). We present a single group design using paired t-tests that demonstrate reduced care burden and increased care satisfaction from pre- to post-participation. Family conflict trended downward after program participation. Findings provide preliminary data to illustrate culturally adapted Alzheimer's disease and related dementia (ADRD) educational programs hold promise to help family members caring for a person living with ADRD, even when such programs are not generally accepted by cultural norms.

Global, regional, and national burdens of Alzheimer's disease and other forms of dementia in the elderly population from 1999 to 2019: A trend analysis based on the Global Burden of Disease Study 2019

AbstractDementia represents a significant health issue, afflicting both patients and their families. To assess the global trends in the incidence, prevalence, mortality, and disability‐adjusted life years (DALYs) of Alzheimer's disease (AD) and other dementias in the elderly population, the Global Burden of Disease Study (1999−2019) was used. The average annual percentage change (AAPC) was estimated using linear regression. Stratified analysis of the global trends by age, sex, region, national level, and social development index (SDI) were also performed. The global incidence of AD and other dementias increased from 507.96 per 100,000 in 1990 to 569.39 per 100,000 in 2019, showing a significant increase in this period. In males, the incidence increased from 387.56 per 100,000 population in 1990 to 462.40 per 100,000 in 2019 (AAPC = 0.61), whereas females experienced a slower rise (AAPC = 0.31) and had a higher incidence in 2019 (662.93 per 100,000 population). The most significant increase was observed in individuals aged 60−64 and those in the middle‐SDI quintile. Regionally, the high‐income Asia Pacific had the highest incidence (890.01 per 100,000 population) and DALYs (3043.86 per 100,000) in AD and other dementias in 2019. As for national trends, Japan had the most pronounced increase in the incidence and DALYs of AD and other dementias during the 1990−2019 period. These findings highlight the growing burden of dementias on life expectancy at a population level, which is significant for healthcare professionals and decision‐makers to conduct the ongoing debate on the policy of AD and other dementias.

Linkage Disequilibrium-Informed Deep Learning Framework to Identify Genetic Loci for Alzheimer's Disease Using Whole Genome Sequencing Data.

The exponential growth of genomic datasets necessitates advanced analytical tools to effectively identify genetic loci from large-scale high throughput sequencing data. This study presents Deep-Block, a multi-stage deep learning framework that incorporates biological knowledge into its AI architecture to identify genetic regions as significantly associated with Alzheimer's disease (AD). The framework employs a three-stage approach: (1) genome segmentation based on linkage disequilibrium (LD) patterns, (2) selection of relevant LD blocks using sparse attention mechanisms, and (3) application of TabNet and Random Forest algorithms to quantify single nucleotide polymorphism (SNP) feature importance, thereby identifying genetic factors contributing to AD risk. The Deep-Block was applied to a large-scale whole genome sequencing (WGS) dataset from the Alzheimer's Disease Sequencing Project (ADSP), comprising 7,416 non-Hispanic white participants (3,150 cognitively normal older adults (CN), 4,266 AD). First, 30,218 LD blocks were identified and then ranked based on their relevance with Alzheimer's disease. Subsequently, the Deep-Block identified novel SNPs within the top 1,500 LD blocks and confirmed previously known variants, including APOE rs429358 and rs769449. The results were cross-validated against established AD-associated loci from the European Alzheimer's and Dementia Biobank (EADB) and the GWAS catalog. The Deep-Block framework effectively processes large-scale high throughput sequencing data while preserving interactions between SNPs in performing the dimensionality reduction, which can potentially introduce bias or lead to information loss. The Deep-Block approach identified both known and novel genetic variation, enhancing our understanding of the genetic architecture of and demonstrating the framework's potential for application in large-scale sequencing studies.

Retinal ganglion cell vulnerability to pathogenic tau in Alzheimer's disease.

Accumulation of pathological tau isoforms, especially hyperphosphorylated tau at serine 396 (pS396-tau) and tau oligomers, has been demonstrated in the retinas of patients with mild cognitive impairment (MCI) and Alzheimer's disease (AD). Previous studies have noted a decrease in retinal ganglion cells (RGCs) in AD patients, but the presence and impact of pathological tau isoforms in RGCs and RGC integrity, particularly in early AD stages, have not been explored. To investigate this, we examined retinal superior temporal cross-sections from 25 patients with MCI (due to AD) or AD dementia and 16 cognitively normal (CN) controls, matched for age and gender. We utilized the RGC marker ribonucleic acid binding protein with multiple splicing (RBPMS) and Nissl staining to assess neuronal density in the ganglion cell layer (GCL). Our study found that hypertrophic RGCs containing pS396-tau and T22-positive tau oligomers were more frequently observed in MCI and AD patients compared to CN subjects. Quantitative analyses indicated a decline in RGC integrity, with 46-55% and 55-56% reductions of RBPMS+ RGCs (P<0.01) and Nissl+ GCL neurons (P<0.01-0.001), respectively, in MCI and AD patients. This decrease in RGC count was accompanied by increases in necroptotic-like morphology and the cleaved caspase-3 apoptotic marker in RGCs of AD patients. Furthermore, there was a 2.1 to 3.1-fold increase (P<0.05-0.0001) in pS396-tau-laden RGCs in MCI and AD patients, with a greater abundance observed in individuals with higher Braak stages (V-VI), more severe clinical dementia ratings (CDR=3), and lower mini-mental state examination (MMSE) scores. Strong correlations were noted between the decline in RGCs and the total amount of retinal pS396-tau and pS396-tau+ RGCs, with pS396-tau+ RGC counts correlating significantly with brain neurofibrillary tangle scores (r= 0.71, P= 0.0001), Braak stage (r= 0.65, P= 0.0009), and MMSE scores (r= -0.76, P= 0.0004). These findings suggest that retinal tauopathy, characterized by pS396-tau and oligomeric tau in hypertrophic RGCs, is associated with and may contribute to RGC degeneration in AD. Future research should validate these findings in larger cohorts and explore noninvasive retinal imaging techniques that target tau pathology in RGCs to improve AD detection and monitor disease progression.

Analysis of Brain Age Gap across Subject Cohorts and Prediction Model Architectures.

Background: Brain age prediction from brain MRI scans and the resulting brain age gap (BAG)-the difference between predicted brain age and chronological age-is a general biomarker for a variety of neurological, psychiatric, and other diseases or disorders. Methods: This study examined the differences in BAG values derived from T1-weighted scans using five state-of-the-art deep learning model architectures previously used in the brain age literature: 2D/3D VGG, RelationNet, ResNet, and SFCN. The models were evaluated on healthy controls and cohorts with sleep apnea, diabetes, multiple sclerosis, Parkinson's disease, mild cognitive impairment, and Alzheimer's disease, employing rigorous statistical analysis, including repeated model training and linear mixed-effects models. Results: All five models consistently identified a statistically significant positive BAG for diabetes (ranging from 0.79 years with RelationNet to 2.13 years with SFCN), multiple sclerosis (2.67 years with 3D VGG to 4.24 years with 2D VGG), mild cognitive impairment (2.13 years with 2D VGG to 2.59 years with 3D VGG), and Alzheimer's dementia (5.54 years with ResNet to 6.48 years with SFCN). For Parkinson's disease, a statistically significant BAG increase was observed in all models except ResNet (1.30 years with 2D VGG to 2.59 years with 3D VGG). For sleep apnea, a statistically significant BAG increase was only detected with the SFCN model (1.59 years). Additionally, we observed a trend of decreasing BAG with increasing chronological age, which was more pronounced in diseased cohorts, particularly those with the largest BAG, such as multiple sclerosis (-0.34 to -0.2), mild cognitive impairment (-0.37 to -0.26), and Alzheimer's dementia (-0.66 to -0.47), compared to healthy controls (-0.18 to -0.1). Conclusions: Consistent with previous research, Alzheimer's dementia and multiple sclerosis exhibited the largest BAG across all models, with SFCN predicting the highest BAG overall. The negative BAG trend suggests a complex interplay of survival bias, disease progression, adaptation, and therapy that influences brain age prediction across the age spectrum.

Subjective cognitive and olfactory impairments predict different prospective dementia outcomes.

Self-reported measures emerge as potential indicators for early detection of dementia and mortality. We investigated the predictive value of different self-reported measures, including subjective cognitive decline (SCD), subjective olfactory impairment (SOI), subjective taste impairment (STI), and self-reported poor health (SPH), in order to determine the risk of progressing to Alzheimer's disease (AD) dementia, Parkinson's disease (PD) dementia, or any-other-cause dementia. A total of 6,028 cognitively unimpaired individuals from the 8th wave of the English Longitudinal Study of Ageing (ELSA) were included as the baseline sample and 5,297 individuals from the 9th wave were included as 2-year follow-up sample. Self-rated measures were assessed using questions from the ELSA structured interview. Three logistic regression models were fitted to predict different the dementia outcomes. SCD based on memory complaints (OR = 11.145; P < 0.001), and older age (OR = 1.108, P < 0.001) significantly predicted the progression to AD dementia at follow-up. SOI (OR = 7.440; P < 0.001) and older age (OR = 1.065, P = 0.035) significantly predicted the progression to PD dementia at follow-up. Furthermore, SCD based on memory complaints (OR = 4.448; P < 0.001) jointly with complaints in other (non-memory) mental abilities (OR = 6.662; P < 0.001), and older age (OR = 1.147, P < 0.001) significantly predicted the progression to dementia of any other cause. Different types of complaints are specifically associated with different dementia outcomes. Our study demonstrates that self-reported measures are a useful and accessible tool when screening for individuals at risk of dementia in the general population.

Clinical value of plasma pTau181 to predict Alzheimer's disease pathology in a large real-world cohort of a memory clinic

BackgroundThe identification of patients with an elevated risk of developing Alzheimer’s disease (AD) dementia and eligible for the disease modifying treatments (DMTs) in the earliest stages is one of the greatest challenges in the clinical practice. Plasma biomarkers has the potential to predict these issues, but further research is still needed to translate them to clinical practice. Here we evaluated the clinical applicability of plasma pTau181 as a predictive marker of AD pathology in a large real-world cohort of a memory clinic. MethodsThree independent cohorts (modelling [n=991, 59.7% female], testing [n=642, 56.2% female] and validation [n=441, 55.1% female]) of real-world patients with subjective cognitive decline (SCD), mild cognitive impairment (MCI), AD dementia, and other dementias were included. Paired cerebrospinal fluid (CSF) and plasma samples were used to measure AT(N) CSF biomarkers and plasma pTau181. FindingsCSF and plasma pTau181 showed correlation in all phenotypes except in SCD and other dementias. Age significantly influenced the biomarker’s performance. The general Aβ(+) vs Aβ(-) ROC curve showed an AUC = 0.77 [0.74 to 0.80], whereas the specific ROC curve of MCI due to AD vs non-AD MCI showed an AUC = 0.89 [0.85 to 0.93]. A cut-off value of 1.30 pg/ml of plasma pTau181 exhibited a sensitivity of 93.57% [88.72 to 96.52], specificity of 72.38 % [62.51 to 79.01], VPP of 77.85% [70.61 to 83.54], and 8.30% false negatives in the subjects with MCI of the testing cohort.The HR of cox regression showed that patients with MCI up to this cut-off value exhibited a HR = 1.84 [1.05 to 3.22] higher risk to convert to AD dementia than patients with MCI below the cut-off value. InterpretationPlasma pTau181 has the potential to be used in the memory clinics as a screening biomarker of AD pathology in subjects with MCI, presenting a valuable prognostic utility in predicting the MCI conversion to AD dementia. In the context of a real-world population, a confirmatory test employing gold-standard procedures is still advisable.Funding: this study has been mainly funded by Ace Alzheimer Center Barcelona, Instituto de Salud Carlos III (ISCIII), Biomedical Research Networking Centre in Neurodegenerative Diseases (CIBERNED), Spanish Ministry of Science and Innovation, Fundación ADEY, Fundación Echevarne and Grífols S.A.

MiR-133b as a potential regulator of a synaptic NPTX2 protein in Alzheimer's disease.

A synaptic protein, Neuronal Pentraxin 2 (NPTX2), has emerged as a pivotal biomarker for Alzheimer's dementia (AD). We identified candidate miRNAs targeting NPTX2 and performed association and mediation analyses using multi-omics data (N = 702). Among 44 candidate miRNAs, miR-133b was significantly associated with AD and Braak positivity. Higher miR-133b expression was also associated with higher NPTX2 gene expression and better cognition. Mediation analysis showed that miR-133b partially influences AD and cognition through the NPTX2 protein. Our integrated approach suggests a potential role of miR-133b in synaptic integrity and offers new insights into AD pathogenesis.

Neuropsychiatric symptoms in cognitive decline and Alzheimer’s disease: biomarker discovery using plasma proteomics

Background and objectivesNeuropsychiatric symptoms (NPS) are common in older people with cognitive impairment and Alzheimer’s disease (AD). No biomarkers to detect the related pathology or predict the clinical evolution of...

FATORES ASSOCIADOS À QUALIDADE DE VIDA DE CUIDADORES DE IDOSOS COM DEMÊNCIA

The objective of this study was to analyze the factors that influence the quality of life of caregivers of elderly people with Alzheimer's dementia. An integrative literature review study was conducted using the secondary databases Virtual Health Library, Latin American and Caribbean Health Sciences Literature, Scientific Electronic Library Online and Online System for Search and Analysis of Medical Literature based on the specific descriptors retrieved in the Health Sciences Descriptors. The factors associated with the quality of life of caregivers of elderly people with Alzheimer's dementia were burden, functional decline and dependence of the elderly to perform activities of daily living, degree of dementia severity, longer time since diagnosis and living with the demented elderly, socioeconomic conditions, psychological stress and decline in social relationships, environment domain, psychological and physical. It is essential that care is also cared for, both from the point of view of health and in relation to public policies of social security and assistance.

Perspectives in the therapeutic management of dementia in Alzheimer's disease

Perspectives in the therapeutic management of dementia in Alzheimer's disease

Considerations for Using Neuroblastoma Cell Lines to Examine the Roles of Iron and Ferroptosis in Neurodegeneration.

Ferroptosis is an iron-dependent form of programmed cell death that is influenced by biological processes such as iron metabolism and senescence. As brain iron levels increase with aging, ferroptosis is also implicated in the development of age-related pathologic conditions such as Alzheimer's disease (AD) and related dementias (ADRD). Indeed, inhibitors of ferroptosis have been shown to be protective in models of degenerative brain disorders like AD/ADRD. Given the inaccessibility of the living human brain for metabolic studies, the goal of this work was to characterize an in vitro model for understanding how aging and iron availability influence neuronal iron metabolism and ferroptosis. First, the human (SH-SY5Y) and mouse (Neuro-2a) neuroblastoma lines were terminally differentiated into mature neurons by culturing in all-trans-retinoic acid for at least 72 h. Despite demonstrating all signs of neuronal differentiation and maturation, including increased expression of the iron storage protein ferritin, we discovered that differentiation conferred ferroptosis resistance in both cell lines. Gene expression data indicates differentiated neurons increase their capacity to protect against iron-mediated oxidative damage by augmenting cystine import, and subsequently increasing intracellular cysteine levels, to promote glutathione production and glutathione peroxidase activity (GPX). In support of this hypothesis, we found that culturing differentiated neurons in cysteine-depleted media sensitized them to GPX4 inhibition, and that these effects are mitigated by cystine supplementation. Such findings are important as they provide guidance for the use of in vitro experimental models to investigate the role of ferroptosis in neurodegeneration in pathologies such as ADRD.

Role of Mitochondrial Dysfunctions in Neurodegenerative Disorders: Advances in Mitochondrial Biology.

Mitochondria, essential organelles responsible for cellular energy production, emerge as a key factor in the pathogenesis of neurodegenerative disorders. This review explores advancements in mitochondrial biology studies that highlight the pivotal connection between mitochondrial dysfunctions and neurological conditions such as Alzheimer's, Parkinson's, Huntington's, ischemic stroke, and vascular dementia. Mitochondrial DNA mutations, impaired dynamics, and disruptions in the ETC contribute to compromised energy production and heightened oxidative stress. These factors, in turn, lead to neuronal damage and cell death. Recent research has unveiled potential therapeutic strategies targeting mitochondrial dysfunction, including mitochondria targeted therapies and antioxidants. Furthermore, the identification of reliable biomarkers for assessing mitochondrial dysfunction opens new avenues for early diagnosis and monitoring of disease progression. By delving into these advancements, this review underscores the significance of understanding mitochondrial biology in unraveling the mechanisms underlying neurodegenerative disorders. It lays the groundwork for developing targeted treatments to combat these devastating neurological conditions.

Neural basis of false recognition in Alzheimer's disease and dementia with lewy bodies.

In Alzheimer's disease (AD), reports on the association between false recognition and brain structure have been inconsistent. In dementia with Lewy bodies (DLB), no such association has been reported. This study aimed to identify brain regions associated with false recognition in AD and DLB by analyzing regional gray matter volume (rGMV). We included 184 patients with AD and 60 patients with DLB. The number of false recognitions was assessed using the Alzheimer's Disease Assessment Scale' word recognition task. Brain regions associated with the number of false recognitions were examined by voxel-based morphometry analysis. The number of false recognitions significantly negatively correlated with rGMV in the bilateral hippocampus, left parahippocampal gyrus, bilateral amygdala, and bilateral entorhinal cortex in patients with AD (p < 0.05, family-wise error [FEW] corrected) and in the bilateral hippocampus, left parahippocampal gyrus, right inferior frontal gyrus, right middle frontal gyrus, right basal forebrain, right insula, left medial and lateral orbital gyri, and left fusiform in those with DLB (p < 0.05, FWE corrected). Bilateral hippocampus and left parahippocampal gyrus were associated with false recognition in both diseases. However, we found there were regions where the association between false recognition and rGMV differed from disease to disease.

Unmet Needs and Factors Impacting Home- and Community-Based Service Use Among Rural Appalachian Caregivers of People With Alzheimer's and Dementia.

Family caregivers of persons with Alzheimer's disease and related dementias (ADRD) living in rural areas face significant health and healthcare challenges. Limited research, however, has explored factors shaping their use of home- and community-based services (HCBS). This study identifies unmet needs among caregivers of people with ADRD in rural Western North Carolina and highlights contextual factors that facilitate HCBS use. Nineteen qualitative interviews were conducted with 21 family caregivers and 1 person with ADRD between 2021 and 2022. Thematic analyses revealed unmet needs among caregivers for information, service navigation, and caregiving support. HCBS use was shaped by multiple factors including illness needs, cultural beliefs, preferences for home-based care, and place-based resources. These findings suggest that culturally tailored HCBS are needed to support people with ADRD and their caregivers in rural Appalachian communities, especially those which facilitate access to paid caregiving, clearly communicate program eligibility requirements, and emphasize service availability.

Proteogenomic signature of risk of Alzheimer's disease and related dementia risk in individuals with a history of major depression disorder.

The mechanisms linking a history of major depressive disorder (MDD) to an increased risk of Alzheimer's disease and related dementia (ADRD) are not fully understood. Using the UK Biobank available proteomic and genomic data, we evaluated the biological mechanisms linking both conditions. In participants with a history of MDD at baseline (n=3,615), we found that plasma levels of NfL, GFAP, PSG1 were associated with higher risk (HR=1.38; 1.37; 1.34, respectively; all adjusted p-values<0.05), while VGF, GET3, and HPGDS were associated with lower risk of incident ADRD (n=150) (HR=0.73; 0.71; 0.66, respectively; all adjusted p-values<0.05) during a mean follow-up of 13.7 years (SD=2.2). Two-sample Mendelian randomization analysis using cis-pQTLs genetic instruments revealed that a lower protein expression of apolipoprotein E and higher IL-10 receptor subunit B were causally linked to incident ADRD. Finally, we developed a Proteomic Risk Score (PrRSMDD-ADRD), which showed strong discriminative power (C-statistic = 0.84) to identify participants with MDD that developed ADRD upon follow-up. In addition to demonstrating an association between plasma proteins associated with inflammation and future ADRD risk in individuals with MDD, our findings include an element of causality using Mendelian Randomization (MR) and PrRSMDD-ADRD can be useful to identify individuals with the highest risk to develop ADRD in a highly vulnerable population.

Associations between misfolded alpha-synuclein aggregates and Alzheimer's disease pathology in vivo.

We examined the relations of misfolded alpha synuclein (α-synuclein) with Alzheimer's disease (AD) biomarkers in two large independent cohorts. We included Biomarkers for Identifying Neurodegenerative Disorders Early and Reliably Two (BioFINDER-2) and Alzheimer's Disease Neuroimaging Initiative (ADNI) participants (n=2315, cognitively unimpaired, mild cognitive impairment, AD dementia) who had cross-sectional cerebrospinal fluid (CSF) α-synuclein measurement from seed-amplification assay as well as cross-sectional and longitudinal amyloid beta (Aβ) and tau levels (measured in CSF and/or by positron emission tomography). All analyses were adjusted for age, sex, and cognitive status. Across cohorts, the main biomarker associated with α-synuclein positivity at baseline was higher levels of Aβ pathology (all p values≤0.02), but not tau. Looking at longitudinal measures of AD biomarkers, α-synuclein -positive participants had a statistically significant faster increase of Aβ load, although of modest magnitude (1.11 Centiloid/year, p=0.02), compared to α-synuclein -negative participants in BioFINDER-2 but not in ADNI. We showed associations between concurrent misfolded α-synuclein and Aβ levels, providing in vivo evidence of links between these two molecular disease pathways in humans. Amyloid beta (Aβ), but not tau, was associated with alpha-synuclein (α-synuclein) positivity. Such association was consistent across two cohorts, beyond the effect of age, sex, and cognitive status. α-synuclein-positive participants had a small, statistically significant faster increase in Aβ positron emission tomography levels in one of the two cohorts.

Obesity, Metabolic Syndrome, and Sugar-Sweetened Beverages (SSBs) in America: A Novel Bioethical Argument for a Radical Public Health Proposal.

The prevalence of obesity, metabolic syndrome, and the associated long-term chronic diseases (cardiovascular disease, type II diabetes, cancer, Alzheimer's disease, depression) have reached epidemic levels in the United States and Western nations. In response to this public health calamity, the author of this paper presents and defends a novel bioethical argument: the consistency argument for outlawing SSBs (sugar-sweetened beverages) for child consumption (the "consistency argument"). This argument's radical conclusion states that the government is justified in outlawing SSBs consumption for child consumption. The reasoning is as follows: if one accepts that the physical harm caused by chronic alcohol consumption justifies the government outlawing alcoholic beverages for child consumption, and there is strong evidence that comparable physical harms result from chronic SSBs consumption, then, mutatis mutandis, the government is also justified in outlawing child consumption of SSBs. To support this argument, the author provides extensive evidence based on epidemiological observational studies, interventional studies, controlled trials, large meta-analyses, and the pathophysiology and biological mechanisms of action behind SSBs and chronic disease. Chronic consumption of large doses of SSBs and alcoholic beverages both drive the same diseases: obesity and insulin resistance, cardiovascular disease, hypertension, and cancer. Chronic SSB consumption carries the additional risk of Alzheimer's disease, dementia, and depression. The author concludes this paper by considering prominent objections to the consistency argument, and then demonstrating that each objection is unsound.

Diagnostic utility of brain MRI volumetry in comparing traumatic brain injury, Alzheimer disease and behavioral variant frontotemporal dementia

BackgroundBrain MRI with volumetric quantification, MRI volumetry, can improve diagnostic delineation of patients with neurocognitive disorders by identifying brain atrophy that may not be evident on visual assessments.ObjectiveTo investigate diagnostic utility of MRI volumetry in traumatic brain injury (TBI), early-onset Alzheimer disease (EOAD), late-onset Alzheimer disease, and behavioral variant frontotemporal dementia (bvFTD).MethodWe utilized 137 participants of TBI (n = 40), EOAD (n = 45), LOAD (n = 32), and bvFTD (n = 20). Participants had 3D T1 brain MRI imaging amendable to MRI volumetry. Scan volumes were analyzed with Neuroreader. One-way ANOVA compared brain volumes across diagnostic groups. Discriminant analysis was done with leave-one-out cross validation on Neuroreader metrics to determine diagnostic delineation across groups.ResultLOAD was the oldest compared to other groups (F = 27.5, p < .001). There were no statistically significant differences in sex (p = .58) with women comprising 54.7% of the entire cohort. EOAD and LOAD had the lowest Mini-Mental State Exam (MMSE) scores compared to TBI (p = .04 for EOAD and p = .01 for LOAD). LOAD had lowest hippocampal volumes (Left Hippocampus F = 13.1, Right Hippocampus F = 7.3, p < .001), low white matter volume in TBI (F = 5.9, p < .001), lower left parietal lobe volume in EOAD (F = 9.4, p < .001), and lower total gray matter volume in bvFTD (F = 32.8, p < .001) and caudate atrophy (F = 1737.5, p < .001). Areas under the curve ranged from 92.3 to 100%, sensitivity between 82.2 and 100%, specificity of 78.1-100%. TBI was the most accurately delineated diagnosis. Predictive features included caudate, frontal, parietal, temporal lobar and total white matter volumes.ConclusionWe identified the diagnostic utility of regional volumetric differences across multiple neurocognitive disorders. Brain MRI volumetry is widely available and can be applied in distinguishing these disorders.