INTRODUCTIONThis study investigated the associations of brain age gap (BAG)—a biological marker of brain resilience—with life exposures, neuroimaging measures, biological processes, and cognitive function.METHODSWe derived BAG by subtracting predicted brain age from chronological age in 739 septuagenarians without dementia or neurological disorders. Robust linear regression models assessed BAG associations

Progressive loss of motor neurons is the hallmark of the neurodegenerative disease amyotrophic lateral sclerosis (ALS), but the underlying disease mechanisms remain incompletely understood. In this study, we investigate the effects of C21ORF2 mutations, a gene recently linked to ALS, and find that primary cilia are dysfunctional. Human patient-derived mutant C21ORF2 motor neurons have a reduced ciliary

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Teng H, Liu Z, Xu J. Surgical treatment for chronic subdural haematoma. Lancet Neurol 2024; 23: 1183–84—In this Correspondence, Jianguo Xu should have been marked as the corresponding author, with the corresponding email address xujg@scu.edu.cn. This correction has been made to the online version as of Dec 18, 2024.

Sheth KN, Albers GW, Saver JL, et al. Intravenous glibenclamide for cerebral oedema after large hemispheric stroke (CHARM): a phase 3, double-blind, placebo-controlled, randomised trial. Lancet Neurol 2024; 23: 1205–13 —In this Article, the CHARM Trial investigators and the appendix have been updated. This correction has been made as of Dec 18, 2024.

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BackgroundSpinal cord injury results in permanent neurological impairment and disability due to the absence of spontaneous regeneration. NG101, a recombinant human antibody, neutralises the neurite growth-inhibiting protein Nogo-A, promoting neural repair and motor recovery in animal models of spinal cord injury. We aimed to evaluate the efficacy of intrathecal NG101 on recovery in patients with acute

BackgroundThe usefulness of current diagnostic approaches in children with suspected autoimmune encephalitis is unknown. We aimed to assess the diagnosis of autoimmune encephalitis in clinical practice and to compare the performance of two international diagnostic algorithms (one intended for patients of any age [general], the other intended for paediatric patients), with particular emphasis on the

Pathogenic variants in the superoxide dismutase 1 (SOD1) gene were the first identified genetic cause of amyotrophic lateral sclerosis (ALS), in 1993. This discovery enabled the development of transgenic rodent models for studying the biology of SOD1 ALS. The understanding that SOD1 ALS is driven by a toxic gain-of-function mutation has led to therapeutic strategies that aim to lower concentrations

Clinical studies have long observed that neurodegenerative disorders display a range of symptoms and pathological features and, in some cases, overlap, suggesting that these diseases exist on a spectrum. Dementia with Lewy Bodies (DLB), a synucleinopathy, is a prominent example, where symptomatic similarities with tauopathy, Alzheimer’s disease, are observed. Although tau pathology has been observed

Alzheimer’s disease (AD) is characterized by the presence of neurofibrillary tangles made of hyperphosphorylated tau and senile plaques composed of beta-amyloid. These pathognomonic deposits have been implicated in the pathogenesis, although the molecular mechanisms and consequences remain undetermined. UFM1 is an important, but understudied ubiquitin-like protein that is covalently attached to substrates

Neuronal oscillations refer to rhythmic and periodic fluctuations of electrical activity in the central nervous system that arise from the cellular properties of diverse neuronal populations and their interactions. Specifically, gamma oscillations play a crucial role in governing the connectivity between distinct brain regions, which are essential in perception, motor control, memory, and emotions

The CD2-associated protein (CD2AP) was initially identified in peripheral immune cells and regulates cytoskeleton and protein trafficking. Single nucleotide polymorphisms (SNPs) in the CD2AP gene have been associated with Alzheimer’s disease (AD). However, the functional role of CD2AP, especially its role in microglia during AD onset, remains elusive. CD2AP protein levels in cultured primary cells

Correction: Mol Neurodegeneration 19, 88 (2024) https://doi.org/10.1186/s13024-024-00779-9 The authors wish to note the Grant ID, MFFF – 007905 relating to the mentioned grants to ZGO and EAF from the Michael J. Fox Foundation which was mistakenly omitted from the original article [1]. The authors also wish to note that Lior Greenbaum is only affiliated to affiliation #14 (Sackler Faculty of Medicine

To understand the potential benefits of emerging Alzheimer's disease (AD) therapies within and beyond clinical trial settings, there is a need to advance current outcome measurements into meaningful information relevant to all stakeholders. The relationship between the impact on disease biology and clinically measurable outcomes in cognition, function, and behavior must be considered when defining

INTRODUCTIONCerebrovascular dysfunction occurs in Alzheimer's disease (AD), impairing hemodynamic regulation. Large conductance Ca2+‐activated K+ channels (BKCa) regulate cerebrovascular reactivity and are impaired in AD. BKCa activity depends on intracellular Ca2+ (Ca2+ sparks) and nitro‐oxidative post‐translational modifications. However, whether these mechanisms underlie BKCa impairment in AD remains

INTRODUCTIONWhile there may be microbial contributions to Alzheimer's disease (AD), findings have been inconclusive. We recently reported an AD‐associated CD83(+) microglia subtype associated with increased immunoglobulin G4 (IgG4) in the transverse colon (TC).METHODSWe used immunohistochemistry (IHC), IgG4 repertoire profiling, and brain organoid experiments to explore this association.RESULTSCD83(+)

BackgroundRecent studies have reported that expanded GCA repeats in the GLS gene can cause glutaminase deficiency with ataxia phenotype. However, to data, no studies have investigated the distribution and role of GCA repeats in the GLS gene of Chinese individuals.ObjectiveThe aim was to investigate the distribution of GCA repeats in Chinese individuals, including undiagnosed ataxia patients for identifying

INTRODUCTIONWe investigated whether early life exposure to state‐level structural sexism influenced late‐life memory trajectories among United Staes (U.S.) ‐born women and men and determined whether associations differed between racialized groups.METHODSParticipants were from the Washington Heights‐Inwood Columbia Aging Project (WHICAP; N = 2314) and Health and Retirement Study (HRS; N = 18,631). State‐level

INTRODUCTIONPlacental growth factor (PlGF) may regulate cerebrovascular permeability. We hypothesized that white matter interstitial fluid accumulation, estimated via magnetic resonance imaging (MRI) free water (FW), would explain the associations between elevated PlGF, white matter hyperintensities (WMH), and cognitive impairment.METHODSMarkVCID consortium participants ≥55 years old with plasma PlGF

The immune system is a key player in the onset and progression of neurodegenerative disorders. While brain resident immune cell‐mediated neuroinflammation and peripheral immune cell (eg, T cell) infiltration into the brain have been shown to significantly contribute to Alzheimer's disease (AD) pathology, the nature and extent of immune responses in the brain in the context of AD and related dementias

INTRODUCTIONStudies using cross‐sectional data or with a short follow‐up period fail to distinguish whether the associations between sleep duration and physical activity with cognitive function result from reverse causation.METHODSThe longitudinal study examined the individual and joint associations, with specific temporality, between sleep duration and physical activity with cognitive function, using

Determining whether disease-modifying treatments (DMTs) in early Alzheimer's disease (AD) provide clinically meaningful benefits to people living with AD is critical and has triggered much debate in the field.1-4 AD is a slowly progressive, ultimately fatal, neurodegenerative disease, characterized by progressive loss in cognitive ability and daily function.5 Current DMTs aim to slow disease progression

Retinoblastoma (RB) proteins are highly conserved transcriptional regulators that play important roles during development by regulating cell-cycle gene expression. RBL2 dysfunction has been linked to a severe neurodevelopmental disorder. However, to date, clinical features have only been described in six individuals carrying five biallelic predicted loss of function (pLOF) variants. To define the phenotypic

BACKGROUND AND OBJECTIVES Despite effective secondary prevention, including oral anticoagulant (OAC) therapy, the risk of recurrent stroke (RS) in patients with atrial fibrillation (AF) remains substantial with an annualized risk of 3.2%-6.5% per year. The reasons for this high residual risk are unclear. There is growing need for improved risk prediction tools to identify patients at greatest risk

BACKGROUND AND OBJECTIVES Sleep disordered breathing (SDB) is a risk factor of stroke and Alzheimer disease and related dementias (ADRDs). Hispanic/Latino adults have higher risk of SDB and ADRDs, which emphasizes the need to better understand the association between SDB and brain health. Furthermore, results on SDB and brain aging are mixed, and there are limited data for Hispanic/Latino adults. The

Backgroundα‐Synuclein seed amplification assay on cerebrospinal fluid (CSF‐αSyn‐SAA) has shown high accuracy for Parkinson's disease (PD) diagnosis. The analysis of CSF‐αSyn‐SAA parameters may provide useful insight to dissect the heterogeneity of synucleinopathies.ObjectiveTo assess differences in CSF‐αSyn‐SAA amplification parameters in participants with PD stratified by rapid eye movement (REM)

In Alzheimer’s disease (AD), the propagation and spreading of CNS tau pathology closely correlates with cognitive decline, positioning tau as an attractive therapeutic target. Amyloid beta (Aβ) has been strongly implicated in driving tau spread, whereas primary tauopathies such as primary age-related tauopathy (PART)—which lack Aβ pathology—exhibit limited tau spread and minimal-to-no cognitive decline

Heart failure (HF) is associated with progressive reduction in cerebral blood flow (CBF) and neurodegenerative changes leading to cognitive decline. The glymphatic system is crucial for the brain's waste removal, and its dysfunction is linked to neurodegeneration. In this study, we used a mouse model of HF, induced by myocardial infarction (MI), to investigate the effects of HF with reduced ejection

Evidence from neuropathological cohorts indicates that a CSF α-synuclein (α-syn) seed amplification assay (SAA) may provide quantitative kinetic parameters correlating with α-syn pathology burden in patients with Lewy body disease (LBD). Studies are needed to assess their longitudinal trend during the pre-symptomatic and clinical disease phases and their correlation with measures of disease progression

BACKGROUND AND OBJECTIVES Facioscapulohumeral dystrophy (FSHD) is an inherited muscle disorder, with childhood onset in 20% of patients. Understanding the natural history of childhood FSHD and identifying clinical and functional outcome measures are crucial for clinical care and future trials. METHODS In a prospective nationwide FSHD cohort study (iFocus), 20 childhood-onset patients were assessed

OBJECTIVES Atypical variants are rare in genetically determined Alzheimer disease (AD). This case describes a patient with Down syndrome-associated Alzheimer disease (DSAD) who presented with symptoms of posterior cortical atrophy (PCA). METHODS We conducted a clinical and cognitive evaluation, APOE genotyping, determination of AD biomarkers in CSF, structural MRI, [18F]FDG-PET, and tau-PET ([18F]PI2620)

BACKGROUND AND OBJECTIVES Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) is the most frequent small artery brain disease caused by pathogenic variants of the NOTCH3 gene. During the disease, we still do not know how the various deficits progress and develop with each other at different stages of the disease. We aim to model disease progression and

Nerve injury causes neuropathic pain and multilevel nerve barrier disruption. Nerve barriers consist of perineurial, endothelial and myelin barriers. So far, it is unclear whether resealing nerve barriers fosters pain resolution and recovery. To this end, we analysed the nerve barrier property portfolio, pain behaviour battery and lipidomics for precursors of specialized pro-resolving meditators (SPMs)