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Citation: Molecular Neurodegeneration 2023 18:34
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Correction: Synaptic dysfunction of Aldh1a1 neurons in the ventral tegmental area causes impulsive behaviors
Citation: Molecular Neurodegeneration 2023 18:33 -
Neuropathology of incidental Lewy body & prodromal Parkinson’s disease
Parkinson’s disease (PD) is a progressive neurodegenerative disorder associated with a loss of dopaminergic (DA) neurons. Despite symptomatic therapies, there is currently no disease-modifying treatment to hal...
Citation: Molecular Neurodegeneration 2023 18:32 -
BACE1 regulates expression of Clusterin in astrocytes for enhancing clearance of β-amyloid peptides
Abnormal accumulation of amyloid beta peptide (Aβ) in the brain induces a cascade of pathological changes in Alzheimer’s disease (AD), and inhibiting BACE1, which is required for Aβ generation, is therefore be...
Citation: Molecular Neurodegeneration 2023 18:31 -
Opinion: more mouse models and more translation needed for ALS
Amyotrophic lateral sclerosis is a complex disorder most of which is ‘sporadic’ of unknown origin but approximately 10% is familial, arising from single mutations in any of more than 30 genes. Thus, there are ...
Citation: Molecular Neurodegeneration 2023 18:30 -
Mutations in α-synuclein, TDP-43 and tau prolong protein half-life through diminished degradation by lysosomal proteases
Autosomal dominant mutations in α-synuclein, TDP-43 and tau are thought to predispose to neurodegeneration by enhancing protein aggregation. While a subset of α-synuclein, TDP-43 and tau mutations has been sho...
Citation: Molecular Neurodegeneration 2023 18:29 -
Correction: Trem2 H157Y increases soluble TREM2 production and reduces amyloid pathology
Citation: Molecular Neurodegeneration 2023 18:28 -
Proteostasis failure exacerbates neuronal circuit dysfunction and sleep impairments in Alzheimer’s disease
Failed proteostasis is a well-documented feature of Alzheimer’s disease, particularly, reduced protein degradation and clearance. However, the contribution of failed proteostasis to neuronal circuit dysfunctio...
Citation: Molecular Neurodegeneration 2023 18:27 -
Leveraging the glymphatic and meningeal lymphatic systems as therapeutic strategies in Alzheimer’s disease: an updated overview of nonpharmacological therapies
Understanding and treating Alzheimer’s disease (AD) has been a remarkable challenge for both scientists and physicians. Although the amyloid-beta and tau protein hypothesis have largely explained the key patho...
Citation: Molecular Neurodegeneration 2023 18:26 -
Carriers of the p.P522R variant in PLCγ2 have a slightly more responsive immune system
The rs72824905 single-nucleotide polymorphism in the PLCG2 gene, encoding the p.P522R residue change in Phospholipase C gamma 2 (PLCγ2), associates with protection against several dementia subtypes and with incre...
Citation: Molecular Neurodegeneration 2023 18:25 -
NF-κB is a critical mediator of post-mitotic senescence in oligodendrocytes and subsequent white matter loss
Inflammaging represents an accepted concept where the immune system shifts to a low-grade chronic pro-inflammatory state without overt infection upon aging. In the CNS, inflammaging is mainly driven by glia ce...
Citation: Molecular Neurodegeneration 2023 18:24 -
Targeting a vulnerable septum-hippocampus cholinergic circuit in a critical time window ameliorates tau-impaired memory consolidation
Abnormal tau accumulation and cholinergic degeneration are hallmark pathologies in the brains of patients with Alzheimer’s disease (AD). However, the sensitivity of cholinergic neurons to AD-like tau accumulat...
Citation: Molecular Neurodegeneration 2023 18:23 -
Using mass spectrometry to validate mouse models of tauopathy
Citation: Molecular Neurodegeneration 2023 18:22 -
Insights from new in vivo models of TREM2 variants
Citation: Molecular Neurodegeneration 2023 18:21 -
Cerebrospinal fluid lipoproteins inhibit α-synuclein aggregation by interacting with oligomeric species in seed amplification assays
Aggregation of α-synuclein (α-syn) is a prominent feature of Parkinson’s disease (PD) and other synucleinopathies. Currently, α-syn seed amplification assays (SAAs) using cerebrospinal fluid (CSF) represent th...
Citation: Molecular Neurodegeneration 2023 18:20 -
hiPSC-based models to decipher the contribution of human astrocytes to Alzheimer’s disease and potential therapeutics
Citation: Molecular Neurodegeneration 2023 18:19 -
Plasma phospho-tau in Alzheimer’s disease: towards diagnostic and therapeutic trial applications
As the leading cause of dementia, Alzheimer's disease (AD) is a major burden on affected individuals, their families and caregivers, and healthcare systems. Although AD can be identified and diagnosed by cereb...
Citation: Molecular Neurodegeneration 2023 18:18 -
Astrocytic APOE4 removal confers cerebrovascular protection despite increased cerebral amyloid angiopathy
Alzheimer Disease (AD) and cerebral amyloid angiopathy (CAA) are both characterized by amyloid-β (Aβ) accumulation in the brain, although Aβ deposits mostly in the brain parenchyma in AD and in the cerebrovasc...
Citation: Molecular Neurodegeneration 2023 18:17 -
The era of cryptic exons: implications for ALS-FTD
TDP-43 is an RNA-binding protein with a crucial nuclear role in splicing, and mislocalises from the nucleus to the cytoplasm in a range of neurodegenerative disorders. TDP-43 proteinopathy spans a spectrum of ...
Citation: Molecular Neurodegeneration 2023 18:16 -
Deficits in mitochondrial TCA cycle and OXPHOS precede rod photoreceptor degeneration during chronic HIF activation
Major retinal degenerative diseases, including age-related macular degeneration, diabetic retinopathy and retinal detachment, are associated with a local decrease in oxygen availability causing the formation o...
Citation: Molecular Neurodegeneration 2023 18:15 -
Correction: Anti-malaria drug artesunate prevents development of amyloid-β pathology in mice by upregulating PICALM at the blood-brain barrier
Citation: Molecular Neurodegeneration 2023 18:14 -
The Alzheimer’s disease-linked protease BACE1 modulates neuronal IL-6 signaling through shedding of the receptor gp130
The protease BACE1 is a major drug target for Alzheimer’s disease, but chronic BACE1 inhibition is associated with non-progressive cognitive worsening that may be caused by modulation of unknown physiological ...
Citation: Molecular Neurodegeneration 2023 18:13 -
A Trem2R47H mouse model without cryptic splicing drives age- and disease-dependent tissue damage and synaptic loss in response to plaques
The TREM2 R47H variant is one of the strongest genetic risk factors for late-onset Alzheimer’s Disease (AD). Unfortunately, many current Trem2 R47H mouse models are associated with cryptic mRNA splicing of the mu...
Citation: Molecular Neurodegeneration 2023 18:12 -
Translational molecular imaging and drug development in Parkinson’s disease
Parkinson’s disease (PD) is a progressive neurodegenerative disorder that primarily affects elderly people and constitutes a major source of disability worldwide. Notably, the neuropathological hallmarks of PD...
Citation: Molecular Neurodegeneration 2023 18:11 -
Common mouse models of tauopathy reflect early but not late human disease
Mouse models that overexpress human mutant Tau (P301S and P301L) are commonly used in preclinical studies of Alzheimer’s Disease (AD) and while several drugs showed therapeutic effects in these mice, they were...
Citation: Molecular Neurodegeneration 2023 18:10 -
The gut microbiome in Alzheimer’s disease: what we know and what remains to be explored
Alzheimer’s disease (AD), the most common cause of dementia, results in a sustained decline in cognition. There are currently few effective disease modifying therapies for AD, but insights into the mechanisms ...
Citation: Molecular Neurodegeneration 2023 18:9 -
Trem2 H157Y increases soluble TREM2 production and reduces amyloid pathology
The rare p.H157Y variant of TREM2 (Triggering Receptor Expressed on Myeloid Cells 2) was found to increase Alzheimer’s disease (AD) risk. This mutation is located at the cleavage site of TREM2 extracellular domai...
Citation: Molecular Neurodegeneration 2023 18:8 -
Anti-malaria drug artesunate prevents development of amyloid-β pathology in mice by upregulating PICALM at the blood-brain barrier
PICALM is one of the most significant susceptibility factors for Alzheimer’s disease (AD). In humans and mice, PICALM is highly expressed in brain endothelium. PICALM endothelial levels are reduced in AD brains. ...
Citation: Molecular Neurodegeneration 2023 18:7 -
In memoriam of Huaxi Xu, PhD, 1964–2022
Citation: Molecular Neurodegeneration 2023 18:6 -
FUS-ALS hiPSC-derived astrocytes impair human motor units through both gain-of-toxicity and loss-of-support mechanisms
Astrocytes play a crucial, yet not fully elucidated role in the selective motor neuron pathology in amyotrophic lateral sclerosis (ALS). Among other responsibilities, astrocytes provide important neuronal home...
Citation: Molecular Neurodegeneration 2023 18:5 -
Advances in sequencing technologies for amyotrophic lateral sclerosis research
Amyotrophic lateral sclerosis (ALS) is caused by upper and lower motor neuron loss and has a fairly rapid disease progression, leading to fatality in an average of 2-5 years after symptom onset. Numerous genes...
Citation: Molecular Neurodegeneration 2023 18:4 -
Alzheimer’s disease: targeting the peripheral circulation
Citation: Molecular Neurodegeneration 2023 18:3 -
Genome-wide association study of brain biochemical phenotypes reveals distinct genetic architecture of Alzheimer’s disease related proteins
Alzheimer’s disease (AD) is neuropathologically characterized by amyloid-beta (Aβ) plaques and neurofibrillary tangles. The main protein components of these hallmarks include Aβ40, Aβ42, tau, phosphor-tau, and...
Citation: Molecular Neurodegeneration 2023 18:2 -
APOE effects on regional tau in preclinical Alzheimer’s disease
APOE variants are strongly associated with abnormal amyloid aggregation and additional direct effects of APOE on tau aggregation are reported in animal and human cell models. The degree to which these effects are...
Citation: Molecular Neurodegeneration 2023 18:1 -
Global neuropathologic severity of Alzheimer’s disease and locus coeruleus vulnerability influences plasma phosphorylated tau levels
Advances in ultrasensitive detection of phosphorylated tau (p-tau) in plasma has enabled the use of blood tests to measure Alzheimer’s disease (AD) biomarker changes. Examination of postmortem brains of partic...
Citation: Molecular Neurodegeneration 2022 17:85 -
TREM2 dependent and independent functions of microglia in Alzheimer’s disease
Microglia are central players in brain innate immunity and have been the subject of extensive research in Alzheimer’s disease (AD). In this review, we aim to summarize the genetic and functional discoveries th...
Citation: Molecular Neurodegeneration 2022 17:84 -
Amyloid-beta and tau pathologies act synergistically to induce novel disease stage-specific microglia subtypes
Amongst risk alleles associated with late-onset Alzheimer’s disease (AD), those that converged on the regulation of microglia activity have emerged as central to disease progression. Yet, how canonical amyloid...
Citation: Molecular Neurodegeneration 2022 17:83 -
Single-cell microglial transcriptomics during demyelination defines a microglial state required for lytic carcass clearance
Microglia regulate the response to injury and disease in the brain and spinal cord. In white matter diseases microglia may cause demyelination. However, how microglia respond and regulate demyelination is not ...
Citation: Molecular Neurodegeneration 2022 17:82 -
Antibody-free measurement of cerebrospinal fluid tau phosphorylation across the Alzheimer’s disease continuum
Alzheimer’s disease is characterized by an abnormal increase of phosphorylated tau (pTau) species in the CSF. It has been suggested that emergence of different pTau forms may parallel disease progression. Ther...
Citation: Molecular Neurodegeneration 2022 17:81 -
Nuclear import receptors are recruited by FG-nucleoporins to rescue hallmarks of TDP-43 proteinopathy
Cytoplasmic mislocalization and aggregation of TAR DNA-binding protein-43 (TDP-43) is a hallmark of the amyotrophic lateral sclerosis and frontotemporal dementia (ALS/FTD) disease spectrum, causing both nuclea...
Citation: Molecular Neurodegeneration 2022 17:80 -
LRP1: a novel receptor for the transmission of pathological α-Synuclein
Citation: Molecular Neurodegeneration 2022 17:79 -
Glial interference: impact of type I interferon in neurodegenerative diseases
Citation: Molecular Neurodegeneration 2022 17:78 -
Multiple system atrophy: α-Synuclein strains at the neuron-oligodendrocyte crossroad
The aberrant accumulation of α-Synuclein within oligodendrocytes is an enigmatic, pathological feature specific to Multiple system atrophy (MSA). Since the characterization of the disease in 1969, decades of r...
Citation: Molecular Neurodegeneration 2022 17:77 -
Upregulation of Ca2+-binding proteins contributes to VTA dopamine neuron survival in the early phases of Alzheimer’s disease in Tg2576 mice
Recent clinical and experimental studies have highlighted the involvement of Ventral Tegmental Area (VTA) dopamine (DA) neurons for the early pathogenesis of Alzheimer’s Disease (AD). We have previously descri...
Citation: Molecular Neurodegeneration 2022 17:76 -
Opposing effects of apoE2 and apoE4 on microglial activation and lipid metabolism in response to demyelination
Abnormal lipid accumulation has been recognized as a key element of immune dysregulation in microglia whose dysfunction contributes to neurodegenerative diseases. Microglia play essential roles in the clearanc...
Citation: Molecular Neurodegeneration 2022 17:75 -
Finding memo: versatile interactions of the VPS10p-Domain receptors in Alzheimer’s disease
The family of VPS10p-Domain (D) receptors comprises five members named SorLA, Sortilin, SorCS1, SorCS2 and SorCS3. While their physiological roles remain incompletely resolved, they have been recognized for th...
Citation: Molecular Neurodegeneration 2022 17:74 -
TREM2 and microglia exosomes: a potential highway for pathological tau
Tau pathology appears to spread along neuronal networks via the template misfolding of tau by pathological tau conformations. The mechanisms underlying neuron-to-neuron transmission of tau are unclear and rece...
Citation: Molecular Neurodegeneration 2022 17:73 -
ApoE in Alzheimer’s disease: pathophysiology and therapeutic strategies
Alzheimer’s disease (AD) is the most common cause of dementia worldwide, and its prevalence is rapidly increasing due to extended lifespans. Among the increasing number of genetic risk factors identified, the ...
Citation: Molecular Neurodegeneration 2022 17:72 -
Correction: Blood-brain barrier-associated pericytes internalize and clear aggregated amyloid-β42 by LRP1-dependent apolipoprotein E isoform-specific mechanism
Citation: Molecular Neurodegeneration 2022 17:71 -
Correction: Challenge accepted: Uncovering the role of rare genetic variants in Alzheimer’s disease
Citation: Molecular Neurodegeneration 2022 17:70
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- ISSN: 1750-1326 (electronic)