Articles
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Citation: Molecular Neurodegeneration 2024 19:39
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Adaptive immune changes associate with clinical progression of Alzheimer’s disease
Alzheimer’s disease (AD) is the most frequent cause of dementia. Recent evidence suggests the involvement of peripheral immune cells in the disease, but the underlying mechanisms remain unclear.
Citation: Molecular Neurodegeneration 2024 19:38 -
Regulation of human microglial gene expression and function via RNAase-H active antisense oligonucleotides in vivo in Alzheimer’s disease
Microglia play important roles in maintaining brain homeostasis and neurodegeneration. The discovery of genetic variants in genes predominately or exclusively expressed in myeloid cells, such as Apolipoprotein...
Citation: Molecular Neurodegeneration 2024 19:37 -
Melatonin: a ferroptosis inhibitor with potential therapeutic efficacy for the post-COVID-19 trajectory of accelerated brain aging and neurodegeneration
The unprecedented pandemic of COVID-19 swept millions of lives in a short period, yet its menace continues among its survivors in the form of post-COVID syndrome. An exponentially growing number of COVID-19 su...
Citation: Molecular Neurodegeneration 2024 19:36 -
Gut microbiota-host lipid crosstalk in Alzheimer’s disease: implications for disease progression and therapeutics
Trillions of intestinal bacteria in the human body undergo dynamic transformations in response to physiological and pathological changes. Alterations in their composition and metabolites collectively contribut...
Citation: Molecular Neurodegeneration 2024 19:35 -
Mitovesicles secreted into the extracellular space of brains with mitochondrial dysfunction impair synaptic plasticity
Hypometabolism tied to mitochondrial dysfunction occurs in the aging brain and in neurodegenerative disorders, including in Alzheimer’s disease, in Down syndrome, and in mouse models of these conditions. We ha...
Citation: Molecular Neurodegeneration 2024 19:34 -
The concept of resilience to Alzheimer’s Disease: current definitions and cellular and molecular mechanisms
Some individuals are able to maintain their cognitive abilities despite the presence of significant Alzheimer’s Disease (AD) neuropathological changes. This discrepancy between cognition and pathology has been...
Citation: Molecular Neurodegeneration 2024 19:33 -
Regulatory T cells limit age-associated retinal inflammation and neurodegeneration
Ageing is the principal risk factor for retinal degenerative diseases, which are the commonest cause of blindness in the developed countries. These conditions include age-related macular degeneration or diabet...
Citation: Molecular Neurodegeneration 2024 19:32 -
An adapted protocol to derive microglia from stem cells and its application in the study of CSF1R-related disorders
Induced pluripotent stem cell-derived microglia (iMGL) represent an excellent tool in studying microglial function in health and disease. Yet, since differentiation and survival of iMGL are highly reliant on c...
Citation: Molecular Neurodegeneration 2024 19:31 -
The endotoxin hypothesis of Alzheimer’s disease
Lipopolysaccharide (LPS) constitutes much of the surface of Gram-negative bacteria, and if LPS enters the human body or brain can induce inflammation and act as an endotoxin. We outline the hypothesis here tha...
Citation: Molecular Neurodegeneration 2024 19:30 -
HDGFL2 cryptic proteins report presence of TDP-43 pathology in neurodegenerative diseases
This letter demonstrates the potential of novel cryptic proteins resulting from TAR DNA-binding protein 43 (TDP-43) dysfunction as markers of TDP-43 pathology in neurodegenerative diseases.
Citation: Molecular Neurodegeneration 2024 19:29 -
Correction: Unravelling cell type-specific responses to Parkinson’s Disease at single cell resolution
Citation: Molecular Neurodegeneration 2024 19:28 -
Correction: Blood–brain barrier-associated pericytes internalize and clear aggregated amyloid-β42 by LRP1-dependent apolipoprotein E isoform-specific mechanism
Citation: Molecular Neurodegeneration 2024 19:27 -
A partial Drp1 knockout improves autophagy flux independent of mitochondrial function
Dynamin-related protein 1 (Drp1) plays a critical role in mitochondrial dynamics. Partial inhibition of this protein is protective in experimental models of neurological disorders such as Parkinson’s disease a...
Citation: Molecular Neurodegeneration 2024 19:26 -
Rejuvenating aged microglia by p16ink4a-siRNA-loaded nanoparticles increases amyloid-β clearance in animal models of Alzheimer’s disease
Age-dependent accumulation of amyloid plaques in patients with sporadic Alzheimer’s disease (AD) is associated with reduced amyloid clearance. Older microglia have a reduced ability to phagocytose amyloid, so ...
Citation: Molecular Neurodegeneration 2024 19:25 -
APOE4 genotype and aging impair injury-induced microglial behavior in brain slices, including toward Aβ, through P2RY12
Microglia are highly dynamic cells that play a critical role in tissue homeostasis through the surveillance of brain parenchyma and response to cues associated with damage. Aging and APOE4 genotype are the strong...
Citation: Molecular Neurodegeneration 2024 19:24 -
Updates on mouse models of Alzheimer’s disease
Alzheimer’s disease (AD) is the most common neurodegenerative disease in the United States (US). Animal models, specifically mouse models have been developed to better elucidate disease mechanisms and test the...
Citation: Molecular Neurodegeneration 2024 19:23 -
GBA1 inactivation in oligodendrocytes affects myelination and induces neurodegenerative hallmarks and lipid dyshomeostasis in mice
Mutations in the β-glucocerebrosidase (GBA1) gene do cause the lysosomal storage Gaucher disease (GD) and are among the most frequent genetic risk factors for Parkinson’s disease (PD). So far, studies on both neu...
Citation: Molecular Neurodegeneration 2024 19:22 -
Correction: The major TMEM106B dementia risk allele affects TMEM106B protein levels, fibril formation, and myelin lipid homeostasis in the ageing human hippocampus
Citation: Molecular Neurodegeneration 2024 19:21 -
Misfolded protein oligomers: mechanisms of formation, cytotoxic effects, and pharmacological approaches against protein misfolding diseases
The conversion of native peptides and proteins into amyloid aggregates is a hallmark of over 50 human disorders, including Alzheimer’s and Parkinson’s diseases. Increasing evidence implicates misfolded protein...
Citation: Molecular Neurodegeneration 2024 19:20 -
Plasma N-terminal containing tau fragments (NTA-tau): a biomarker of tau deposition in Alzheimer’s Disease
Novel phosphorylated-tau (p-tau) blood biomarkers (e.g., p-tau181, p-tau217 or p-tau231), are highly specific for Alzheimer’s disease (AD), and can track amyloid-β (Aβ) and tau pathology. However, because thes...
Citation: Molecular Neurodegeneration 2024 19:19 -
Sodium oligomannate alters gut microbiota, reduces cerebral amyloidosis and reactive microglia in a sex-specific manner
It has recently become well-established that there is a connection between Alzheimer’s disease pathology and gut microbiome dysbiosis. We have previously demonstrated that antibiotic-mediated gut microbiota pe...
Citation: Molecular Neurodegeneration 2024 19:18 -
Correction: Collusion of α-Synuclein and Aβ aggravating co-morbidities in a novel prion-type mouse model
Citation: Molecular Neurodegeneration 2024 19:17 -
Unraveling the dual nature of brain CD8+ T cells in Alzheimer’s disease
Citation: Molecular Neurodegeneration 2024 19:16 -
CSF protein ratios with enhanced potential to reflect Alzheimer’s disease pathology and neurodegeneration
Amyloid and tau aggregates are considered to cause neurodegeneration and consequently cognitive decline in individuals with Alzheimer’s disease (AD). Here, we explore the potential of cerebrospinal fluid (CSF)...
Citation: Molecular Neurodegeneration 2024 19:15 -
Cognitive, functional, and neuropsychiatric correlates of regional tau pathology in autopsy-confirmed chronic traumatic encephalopathy
Chronic traumatic encephalopathy (CTE) is a neurodegenerative disease characterized by hyperphosphorylated tau (p-tau) accumulation. The clinical features associated with CTE pathology are unclear. In brain do...
Citation: Molecular Neurodegeneration 2024 19:10 -
Microglial ferroptotic stress causes non-cell autonomous neuronal death
Ferroptosis is a form of regulated cell death characterised by lipid peroxidation as the terminal endpoint and a requirement for iron. Although it protects against cancer and infection, ferroptosis is also imp...
Citation: Molecular Neurodegeneration 2024 19:14 -
NMNAT2 supports vesicular glycolysis via NAD homeostasis to fuel fast axonal transport
Bioenergetic maladaptations and axonopathy are often found in the early stages of neurodegeneration. Nicotinamide adenine dinucleotide (NAD), an essential cofactor for energy metabolism, is mainly synthesized ...
Citation: Molecular Neurodegeneration 2024 19:13 -
Mitochondrial CISD1/Cisd accumulation blocks mitophagy and genetic or pharmacological inhibition rescues neurodegenerative phenotypes in Pink1/parkin models
Mitochondrial dysfunction and toxic protein aggregates have been shown to be key features in the pathogenesis of neurodegenerative diseases, such as Parkinson’s disease (PD). Functional analysis of genes linke...
Citation: Molecular Neurodegeneration 2024 19:12 -
Collagen in the central nervous system: contributions to neurodegeneration and promise as a therapeutic target
The extracellular matrix is a richly bioactive composition of substrates that provides biophysical stability, facilitates intercellular signaling, and both reflects and governs the physiological status of the ...
Citation: Molecular Neurodegeneration 2024 19:11 -
Fluid biomarkers for amyotrophic lateral sclerosis: a review
Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disease characterized by the loss of upper and lower motor neurons. Presently, three FDA-approved drugs are available to help slow functional de...
Citation: Molecular Neurodegeneration 2024 19:9 -
Nuclear-import receptors as gatekeepers of pathological phase transitions in ALS/FTD
Amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD) are fatal neurodegenerative disorders on a disease spectrum that are characterized by the cytoplasmic mislocalization and aberrant phase tr...
Citation: Molecular Neurodegeneration 2024 19:8 -
Unravelling cell type-specific responses to Parkinson’s Disease at single cell resolution
Parkinson’s Disease (PD) is the second most common neurodegenerative disorder. The pathological hallmark of PD is loss of dopaminergic neurons and the presence of aggregated α-synuclein, primarily in the subst...
Citation: Molecular Neurodegeneration 2024 19:7 -
Real-time imaging of mitochondrial redox reveals increased mitochondrial oxidative stress associated with amyloid β aggregates in vivo in a mouse model of Alzheimer’s disease
Reactive oxidative stress is a critical player in the amyloid beta (Aβ) toxicity that contributes to neurodegeneration in Alzheimer’s disease (AD). Damaged mitochondria are one of the main sources of reactive ...
Citation: Molecular Neurodegeneration 2024 19:6 -
Brain clearance of protein aggregates: a close-up on astrocytes
Protein misfolding and accumulation defines a prevailing feature of many neurodegenerative disorders, finally resulting in the formation of toxic intra- and extracellular aggregates. Intracellular aggregates c...
Citation: Molecular Neurodegeneration 2024 19:5 -
Neuronal and glial vulnerability of the suprachiasmatic nucleus in tauopathies: evidence from human studies and animal models
Tauopathies, a group of neurodegenerative diseases that includes Alzheimer’s disease, commonly lead to disturbances in sleep-wake patterns and circadian rhythm disorders. The circadian rhythm, a recurring 24-h...
Citation: Molecular Neurodegeneration 2024 19:4 -
Blood platelet factor 4: the elixir of brain rejuvenation
Citation: Molecular Neurodegeneration 2024 19:3 -
Comparison of immunoassay- with mass spectrometry-derived p-tau quantification for the detection of Alzheimer’s disease pathology
Antibody-based immunoassays have enabled quantification of very low concentrations of phosphorylated tau (p-tau) protein forms in cerebrospinal fluid (CSF), aiding in the diagnosis of AD. Mass spectrometry ena...
Citation: Molecular Neurodegeneration 2024 19:2 -
Proteo-genomics of soluble TREM2 in cerebrospinal fluid provides novel insights and identifies novel modulators for Alzheimer’s disease
Triggering receptor expressed on myeloid cells 2 (TREM2) plays a critical role in microglial activation, survival, and apoptosis, as well as in Alzheimer’s disease (AD) pathogenesis. We previously reported the MS...
Citation: Molecular Neurodegeneration 2024 19:1 -
Untargeted serum metabolomics reveals novel metabolite associations and disruptions in amino acid and lipid metabolism in Parkinson’s disease
Untargeted high-resolution metabolomic profiling provides simultaneous measurement of thousands of metabolites. Metabolic networks based on these data can help uncover disease-related perturbations across inte...
Citation: Molecular Neurodegeneration 2023 18:100 -
Microglial APOE4: more is less and less is more
Apolipoprotein E (APOE) is the single greatest genetic risk factor for late onset Alzheimer’s disease (AD). Yet, the cell-specific effects of APOE on microglia function have remained unclear. Fortunately, two ...
Citation: Molecular Neurodegeneration 2023 18:99 -
Advanced structural brain aging in preclinical autosomal dominant Alzheimer disease
“Brain-predicted age” estimates biological age from complex, nonlinear features in neuroimaging scans. The brain age gap (BAG) between predicted and chronological age is elevated in sporadic Alzheimer disease ...
Citation: Molecular Neurodegeneration 2023 18:98 -
Amyloid-β specific regulatory T cells attenuate Alzheimer’s disease pathobiology in APP/PS1 mice
Regulatory T cells (Tregs) maintain immune tolerance. While Treg-mediated neuroprotective activities are now well-accepted, the lack of defined antigen specificity limits their therapeutic potential. This is n...
Citation: Molecular Neurodegeneration 2023 18:97 -
Correction: Multi-modal proteomic characterization of lysosomal function and proteostasis in progranulin-deficient neurons
Citation: Molecular Neurodegeneration 2023 18:96 -
Translational profiling identifies sex-specific metabolic and epigenetic reprogramming of cortical microglia/macrophages in APPPS1-21 mice with an antibiotic-perturbed-microbiome
Microglia, the brain-resident macrophages perform immune surveillance and engage with pathological processes resulting in phenotype changes necessary for maintaining homeostasis. In preceding studies, we showe...
Citation: Molecular Neurodegeneration 2023 18:95 -
MLKL deficiency alleviates neuroinflammation and motor deficits in the α-synuclein transgenic mouse model of Parkinson’s disease
Parkinson’s disease (PD), one of the most devastating neurodegenerative brain disorders, is characterized by the progressive loss of dopaminergic neurons in the substantia nigra (SN) and deposits of α-synuclei...
Citation: Molecular Neurodegeneration 2023 18:94 -
Sleep restoration by optogenetic targeting of GABAergic neurons reprograms microglia and ameliorates pathological phenotypes in an Alzheimer’s disease model
Alzheimer’s disease (AD) patients exhibit memory disruptions and profound sleep disturbances, including disruption of deep non-rapid eye movement (NREM) sleep. Slow-wave activity (SWA) is a major restorative f...
Citation: Molecular Neurodegeneration 2023 18:93 -
Microglial function, INPP5D/SHIP1 signaling, and NLRP3 inflammasome activation: implications for Alzheimer’s disease
Recent genetic studies on Alzheimer’s disease (AD) have brought microglia under the spotlight, as loci associated with AD risk are enriched in genes expressed in microglia. Several of these genes have been rec...
Citation: Molecular Neurodegeneration 2023 18:89 -
Characterization of APOE Christchurch carriers in 455,306 UK Biobank participants
Citation: Molecular Neurodegeneration 2023 18:92 -
Non-invasive systemic viral delivery of human alpha-synuclein mimics selective and progressive neuropathology of Parkinson’s disease in rodent brains
Alpha-synuclein (α-syn) aggregation into proteinaceous intraneuronal inclusions, called Lewy bodies (LBs), is the neuropathological hallmark of Parkinson’s disease (PD) and related synucleinopathies. However, ...
Citation: Molecular Neurodegeneration 2023 18:91
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- ISSN: 1750-1326 (electronic)