Acta Neuropathologica

(The TQCC of Acta Neuropathologica is 60. The table below lists those papers that are above that threshold based on CrossRef citation counts. The publications cover those that have been published in the past four years, i.e., from 2019-03-01 to 2023-03-01.)
The first NINDS/NIBIB consensus meeting to define neuropathological criteria for the diagnosis of chronic traumatic encephalopathy545
Functional morphology of the blood–brain barrier in health and disease392
Aging-related tau astrogliopathy (ARTAG): harmonized evaluation strategy318
White matter injury in the preterm infant: pathology and mechanisms207
Post-stroke inflammation—target or tool for therapy?205
Chronic traumatic encephalopathy pathology in a neurodegenerative disorders brain bank190
Beta-amyloid deposition in chronic traumatic encephalopathy182
Quantitative analysis and clinico-pathological correlations of different dipeptide repeat protein pathologies in C9ORF72 mutation carriers177
Neurotropic virus infections as the cause of immediate and delayed neuropathology175
Aggregated Tau activates NLRP3–ASC inflammasome exacerbating exogenously seeded and non-exogenously seeded Tau pathology in vivo174
Neurotoxicity of pesticides169
Evidence for bidirectional and trans-synaptic parasympathetic and sympathetic propagation of alpha-synuclein in rats165
Endocytic vesicle rupture is a conserved mechanism of cellular invasion by amyloid proteins161
α-Synuclein transfer between neurons and astrocytes indicates that astrocytes play a role in degradation rather than in spreading153
Presynaptic dystrophic neurites surrounding amyloid plaques are sites of microtubule disruption, BACE1 elevation, and increased Aβ generation in Alzheimer’s disease151
The pathology of central nervous system inflammatory demyelinating disease accompanying myelin oligodendrocyte glycoprotein autoantibody143
Dissecting the genetic basis of focal cortical dysplasia: a large cohort study139
Inflammation in ALS/FTD pathogenesis138
cIMPACT-NOW update 4: diffuse gliomas characterized by MYB, MYBL1, or FGFR1 alterations or BRAFV600E mutation130
Galectin-3, a novel endogenous TREM2 ligand, detrimentally regulates inflammatory response in Alzheimer’s disease128
The contribution of astrocytes to the neuroinflammatory response in multiple sclerosis and experimental autoimmune encephalomyelitis126
Spread of aggregates after olfactory bulb injection of α-synuclein fibrils is associated with early neuronal loss and is reduced long term126
Second-generation molecular subgrouping of medulloblastoma: an international meta-analysis of Group 3 and Group 4 subtypes124
Microglial cell loss after ischemic stroke favors brain neutrophil accumulation121
Rapid lymphatic efflux limits cerebrospinal fluid flow to the brain102
Prion-like propagation of mutant SOD1 misfolding and motor neuron disease spread along neuroanatomical pathways101
The new genetic landscape of Alzheimer’s disease: from amyloid cascade to genetically driven synaptic failure hypothesis?101
LRRK2 modifies α-syn pathology and spread in mouse models and human neurons101
The complexity of neuroinflammation consequent to traumatic brain injury: from research evidence to potential treatments100
The origin, fate, and contribution of macrophages to spinal cord injury pathology99
The structural differences between patient-derived α-synuclein strains dictate characteristics of Parkinson’s disease, multiple system atrophy and dementia with Lewy bodies96
From the prion-like propagation hypothesis to therapeutic strategies of anti-tau immunotherapy96
Novel tau fragments in cerebrospinal fluid: relation to tangle pathology and cognitive decline in Alzheimer’s disease95
The role of ABCA7 in Alzheimer’s disease: evidence from genomics, transcriptomics and methylomics91
Detrimental and protective action of microglial extracellular vesicles on myelin lesions: astrocyte involvement in remyelination failure88
Picomolar concentrations of oligomeric alpha-synuclein sensitizes TLR4 to play an initiating role in Parkinson’s disease pathogenesis85
Spinal poly-GA inclusions in a C9orf72 mouse model trigger motor deficits and inflammation without neuron loss85
PrP is a central player in toxicity mediated by soluble aggregates of neurodegeneration-causing proteins85
Neurotoxicity of polychlorinated biphenyls and related organohalogens84
Disrupted neuronal trafficking in amyotrophic lateral sclerosis81
Cerebellar c9RAN proteins associate with clinical and neuropathological characteristics of C9ORF72 repeat expansion carriers80
α-Synuclein and astrocytes: tracing the pathways from homeostasis to neurodegeneration in Lewy body disease77
FUS pathology in ALS is linked to alterations in multiple ALS-associated proteins and rescued by drugs stimulating autophagy75
Tau drives translational selectivity by interacting with ribosomal proteins73
Molecular profiling of tumors of the brainstem by sequencing of CSF-derived circulating tumor DNA73
Dissecting the genetic relationship between cardiovascular risk factors and Alzheimer’s disease73
Seeding selectivity and ultrasensitive detection of tau aggregate conformers of Alzheimer disease72
Precise detection of low-level somatic mutation in resected epilepsy brain tissue71
Dihydropyridine receptor (DHPR, CACNA1S) congenital myopathy71
An update on the CNS manifestations of neurofibromatosis type 270
C9orf72 arginine-rich dipeptide proteins interact with ribosomal proteins in vivo to induce a toxic translational arrest that is rescued by eIF1A69
Epigenetic loss of RNA-methyltransferase NSUN5 in glioma targets ribosomes to drive a stress adaptive translational program68
4-Repeat tau seeds and templating subtypes as brain and CSF biomarkers of frontotemporal lobar degeneration68
MYCN amplification drives an aggressive form of spinal ependymoma66
Necrosome complex detected in granulovacuolar degeneration is associated with neuronal loss in Alzheimer’s disease64
A nonsynonymous mutation in PLCG2 reduces the risk of Alzheimer’s disease, dementia with Lewy bodies and frontotemporal dementia, and increases the likelihood of longevity64
Depopulation of dense α-synuclein aggregates is associated with rescue of dopamine neuron dysfunction and death in a new Parkinson’s disease model62
Chronic traumatic encephalopathy is a common co-morbidity, but less frequent primary dementia in former soccer and rugby players61
Genome-wide analyses as part of the international FTLD-TDP whole-genome sequencing consortium reveals novel disease risk factors and increases support for immune dysfunction in FTLD61
H3.3 K27M depletion increases differentiation and extends latency of diffuse intrinsic pontine glioma growth in vivo60