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Citation: Molecular Neurodegeneration 2022 17:71
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Correction: Challenge accepted: Uncovering the role of rare genetic variants in Alzheimer’s disease
Citation: Molecular Neurodegeneration 2022 17:70 -
Common features of neurodegenerative disease: exploring the brain-eye connection and beyond (part 2): the 2021 pre-symposium of the 15th international conference on Alzheimer’s and Parkinson’s diseases
Citation: Molecular Neurodegeneration 2022 17:69 -
Common features of neurodegenerative disease: exploring the brain-eye connection and beyond (Part 1): the 2021 pre-symposium of the 15th international conference on Alzheimer’s and Parkinson’s diseases
Citation: Molecular Neurodegeneration 2022 17:68 -
The Golgi apparatus: Site for convergence of COVID-19 brain fog and Alzheimer’s disease?
Citation: Molecular Neurodegeneration 2022 17:67 -
Tau interactome and RNA binding proteins in neurodegenerative diseases
Pathological tau aggregation is a primary neuropathological feature of many neurodegenerative diseases. Intriguingly, despite the common presence of tau aggregates in these diseases the affected brain regions,...
Citation: Molecular Neurodegeneration 2022 17:66 -
Liver-ing in your head rent free: peripheral ApoE4 drives CNS pathology
Citation: Molecular Neurodegeneration 2022 17:65 -
Author response to “post-infection cognitive impairments in a cohort of elderly patients with COVID-19”
Citation: Molecular Neurodegeneration 2022 17:64 -
To the editor: Response to post-infection cognitive impairments in a cohort of elderly patients with COVID-19, by Wang, Y.J. et al. (2021)
Citation: Molecular Neurodegeneration 2022 17:63 -
APOE in the bullseye of neurodegenerative diseases: impact of the APOE genotype in Alzheimer’s disease pathology and brain diseases
ApoE is the major lipid and cholesterol carrier in the CNS. There are three major human polymorphisms, apoE2, apoE3, and apoE4, and the genetic expression of APOE4 is one of the most influential risk factors for ...
Citation: Molecular Neurodegeneration 2022 17:62 -
Elevated ganglioside GM2 activator (GM2A) in human brain tissue reduces neurite integrity and spontaneous neuronal activity
Alzheimer’s Disease (AD) affects millions globally, but therapy development is lagging. New experimental systems that monitor neuronal functions in conditions approximating the AD brain may be beneficial for i...
Citation: Molecular Neurodegeneration 2022 17:61 -
Aging exacerbates the brain inflammatory micro-environment contributing to α-synuclein pathology and functional deficits in a mouse model of DLB/PD
Although ɑ-synuclein (ɑ-syn) spreading in age-related neurodegenerative diseases such as Parkinson’s disease (PD) and Dementia with Lewy bodies (DLB) has been extensively investigated, the role of aging in the...
Citation: Molecular Neurodegeneration 2022 17:60 -
CD8+ T cells in neurodegeneration: friend or foe?
Citation: Molecular Neurodegeneration 2022 17:59 -
Trem2 deletion enhances tau dispersion and pathology through microglia exosomes
Alzheimer’s disease (AD) is a neurodegenerative disorder that manifests sequential Aβ and tau brain pathology with age-dependent onset. Variants in the microglial immune receptor TREM2 are associated with enha...
Citation: Molecular Neurodegeneration 2022 17:58 -
LRP1 is a neuronal receptor for α-synuclein uptake and spread
The aggregation and spread of α-synuclein (α-Syn) protein and related neuronal toxicity are the key pathological features of Parkinson’s disease (PD) and Lewy body dementia (LBD). Studies have shown that patho...
Citation: Molecular Neurodegeneration 2022 17:57 -
Correction: Alzheimer risk gene product Pyk2 suppresses tau phosphorylation and phenotypic effects of tauopathy
Citation: Molecular Neurodegeneration 2022 17:56 -
Microglial TYROBP/DAP12 in Alzheimer’s disease: Transduction of physiological and pathological signals across TREM2
TYROBP (also known as DAP12 or KARAP) is a transmembrane adaptor protein initially described as a receptor-activating subunit component of natural killer (NK) cells. TYROBP is expressed in numerous cell types,...
Citation: Molecular Neurodegeneration 2022 17:55 -
Farnesyltransferase inhibitor LNK-754 attenuates axonal dystrophy and reduces amyloid pathology in mice
Amyloid plaque deposition and axonal degeneration are early events in AD pathogenesis. Aβ disrupts microtubules in presynaptic dystrophic neurites, resulting in the accumulation of impaired endolysosomal and a...
Citation: Molecular Neurodegeneration 2022 17:54 -
When the infectious environment meets the AD brain
The Amyloid theory of Alzheimer’s disease (AD) suggests that the deposition of Amyloid β (Aβ) in the brain triggers a chain of events, involving the deposition of phosphorylated Tau and other misfolded protein...
Citation: Molecular Neurodegeneration 2022 17:53 -
Transcriptome deregulation of peripheral monocytes and whole blood in GBA-related Parkinson’s disease
Genetic mutations in beta-glucocerebrosidase (GBA) represent the major genetic risk factor for Parkinson’s disease (PD). GBA participates in both the endo-lysosomal pathway and the immune response, two important ...
Citation: Molecular Neurodegeneration 2022 17:52 -
APOE targeting strategy in Alzheimer’s disease: lessons learned from protective variants
Citation: Molecular Neurodegeneration 2022 17:51 -
Crosstalk of organelles in Parkinson’s disease – MiT family transcription factors as central players in signaling pathways connecting mitochondria and lysosomes
Living organisms constantly need to adapt to their surrounding environment and have evolved sophisticated mechanisms to deal with stress. Mitochondria and lysosomes are central organelles in the response to en...
Citation: Molecular Neurodegeneration 2022 17:50 -
Combination therapy using GDNF and cell transplant in Parkinson’s disease
Citation: Molecular Neurodegeneration 2022 17:49 -
17q21.31 sub-haplotypes underlying H1-associated risk for Parkinson’s disease are associated with LRRC37A/2 expression in astrocytes
Parkinson’s disease (PD) is genetically associated with the H1 haplotype of the MAPT 17q.21.31 locus, although the causal gene and variants underlying this association have not been identified.
Citation: Molecular Neurodegeneration 2022 17:48 -
CX3CR1 deficiency aggravates amyloid driven neuronal pathology and cognitive decline in Alzheimer’s disease
Despite its identification as a key checkpoint regulator of microglial activation in Alzheimer’s disease, the overarching role of CX3CR1 signaling in modulating mechanisms of Aβ driven neurodegeneration, inclu...
Citation: Molecular Neurodegeneration 2022 17:47 -
The role of NURR1 in metabolic abnormalities of Parkinson’s disease
A constant metabolism and energy supply are crucial to all organs, particularly the brain. Age-dependent neurodegenerative diseases, such as Parkinson’s disease (PD), are associated with alterations in cellula...
Citation: Molecular Neurodegeneration 2022 17:46 -
Unraveling protein dynamics to understand the brain – the next molecular frontier
The technological revolution to measure global gene expression at the single-cell level is currently transforming our knowledge of the brain and neurological diseases, leading from a basic understanding of gen...
Citation: Molecular Neurodegeneration 2022 17:45 -
LILRB2-mediated TREM2 signaling inhibition suppresses microglia functions
Microglia plays crucial roles in Alzheimer’s disease (AD) development. Triggering receptor expressed on myeloid cells 2 (TREM2) in association with DAP12 mediates signaling affecting microglia function. Here w...
Citation: Molecular Neurodegeneration 2022 17:44 -
Microbial-derived metabolites as a risk factor of age-related cognitive decline and dementia
A consequence of our progressively ageing global population is the increasing prevalence of worldwide age-related cognitive decline and dementia. In the absence of effective therapeutic interventions, identify...
Citation: Molecular Neurodegeneration 2022 17:43 -
Calcium-dependent cytosolic phospholipase A2 activation is implicated in neuroinflammation and oxidative stress associated with ApoE4
Apolipoprotein E4 (APOE4) is associated with a greater response to neuroinflammation and the risk of developing late-onset Alzheimer’s disease (AD), but the mechanisms for this association are not clear. The acti...
Citation: Molecular Neurodegeneration 2022 17:42 -
Novel App knock-in mouse model shows key features of amyloid pathology and reveals profound metabolic dysregulation of microglia
Genetic mutations underlying familial Alzheimer’s disease (AD) were identified decades ago, but the field is still in search of transformative therapies for patients. While mouse models based on overexpression...
Citation: Molecular Neurodegeneration 2022 17:41 -
TREM2 in the pathogenesis of AD: a lipid metabolism regulator and potential metabolic therapeutic target
Triggering receptor expressed on myeloid cells 2 (TREM2) is a single-pass transmembrane immune receptor that is mainly expressed on microglia in the brain and macrophages in the periphery. Recent studies have ...
Citation: Molecular Neurodegeneration 2022 17:40 -
Imaging tau pathology in Alzheimer’s disease with positron emission tomography: lessons learned from imaging-neuropathology validation studies
Citation: Molecular Neurodegeneration 2022 17:39 -
Prompting endogenous repair of brain injury: science fiction or reality?
Drug-refractory forms of neurological diseases could find their next breakthrough therapy in non-pharmacological approaches to brain repair. Lentini et al. present the potential of in situ brain regeneration to a...
Citation: Molecular Neurodegeneration 2022 17:38 -
Correction: Cerebrospinal fluid tau levels are associated with abnormal neuronal plasticity markers in Alzheimer’s disease
Citation: Molecular Neurodegeneration 2022 17:37 -
Microglial lactate metabolism as a potential therapeutic target for Alzheimer’s disease
Citation: Molecular Neurodegeneration 2022 17:36 -
Circadian clocks, cognition, and Alzheimer’s disease: synaptic mechanisms, signaling effectors, and chronotherapeutics
Modulation of basic biochemical and physiological processes by the circadian timing system is now recognized as a fundamental feature of all mammalian organ systems. Within the central nervous system, these cl...
Citation: Molecular Neurodegeneration 2022 17:35 -
Oligodendrocyte death and myelin loss in the cuprizone model: an updated overview of the intrinsic and extrinsic causes of cuprizone demyelination
The dietary consumption of cuprizone – a copper chelator – has long been known to induce demyelination of specific brain structures and is widely used as model of multiple sclerosis. Despite the extensive use ...
Citation: Molecular Neurodegeneration 2022 17:34 -
BIN1 is a key regulator of proinflammatory and neurodegeneration-related activation in microglia
The BIN1 locus contains the second-most significant genetic risk factor for late-onset Alzheimer’s disease. BIN1 undergoes alternate splicing to generate tissue- and cell-type-specific BIN1 isoforms, which regula...
Citation: Molecular Neurodegeneration 2022 17:33 -
Alzheimer risk gene product Pyk2 suppresses tau phosphorylation and phenotypic effects of tauopathy
Genetic variation at the PTK2B locus encoding the protein Pyk2 influences Alzheimer’s disease risk. Neurons express Pyk2 and the protein is required for Amyloid-β (Aβ) peptide driven deficits of synaptic function...
Citation: Molecular Neurodegeneration 2022 17:32 -
The role of ATP-binding cassette subfamily A in the etiology of Alzheimer’s disease
Alzheimer’s disease (AD) is the leading cause of dementia, clinically characterized by memory deficits and progressive cognitive decline. Despite decades of research effective therapies are lacking, and a larg...
Citation: Molecular Neurodegeneration 2022 17:31 -
VCP suppresses proteopathic seeding in neurons
Neuronal uptake and subsequent spread of proteopathic seeds, such as αS (alpha-synuclein), Tau, and TDP-43, contribute to neurodegeneration. The cellular machinery participating in this process is poorly under...
Citation: Molecular Neurodegeneration 2022 17:30 -
Multimarker synaptic protein cerebrospinal fluid panels reflect TDP-43 pathology and cognitive performance in a pathological cohort of frontotemporal lobar degeneration
Synapse degeneration is an early event in pathological frontotemporal lobar degeneration (FTLD). Consequently, a surrogate marker of synapse loss could be used to monitor early pathologic changes in patients w...
Citation: Molecular Neurodegeneration 2022 17:29 -
Tauopathies: new perspectives and challenges
Tauopathies are a class of neurodegenerative disorders characterized by neuronal and/or glial tau-positive inclusions.
Citation: Molecular Neurodegeneration 2022 17:28 -
Cerebrospinal fluid tau levels are associated with abnormal neuronal plasticity markers in Alzheimer’s disease
Increased total tau (t-tau) in cerebrospinal fluid (CSF) is a key characteristic of Alzheimer’s disease (AD) and is considered to result from neurodegeneration. T-tau levels, however, can be increased in very ...
Citation: Molecular Neurodegeneration 2022 17:27 -
Culture shock: microglial heterogeneity, activation, and disrupted single-cell microglial networks in vitro
Microglia, the resident immune cells of the brain, play a critical role in numerous diseases, but are a minority cell type and difficult to genetically manipulate in vivo with viral vectors and other approache...
Citation: Molecular Neurodegeneration 2022 17:26 -
Cellular stress signaling and the unfolded protein response in retinal degeneration: mechanisms and therapeutic implications
The retina, as part of the central nervous system (CNS) with limited capacity for self-reparation and regeneration in mammals, is under cumulative environmental stress due to high-energy demands and rapid prot...
Citation: Molecular Neurodegeneration 2022 17:25 -
In Memoriam of John T. Trojanowski, MD, PhD 1946-2022
Citation: Molecular Neurodegeneration 2022 17:24 -
Solving neurodegeneration: common mechanisms and strategies for new treatments
Across neurodegenerative diseases, common mechanisms may reveal novel therapeutic targets based on neuronal protection, repair, or regeneration, independent of etiology or site of disease pathology. To address...
Citation: Molecular Neurodegeneration 2022 17:23 -
The role of inflammation in neurodegeneration: novel insights into the role of the immune system in C9orf72 HRE-mediated ALS/FTD
Neuroinflammation is an important hallmark of amyotrophic lateral sclerosis (ALS) and frontotemporal lobar degeneration (FTLD). An inflammatory reaction to neuronal injury is deemed vital for neuronal health a...
Citation: Molecular Neurodegeneration 2022 17:22
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- ISSN: 1750-1326 (electronic)