Impact Factor
4.77
Journal Citation Impact
Estimated influence, citation density, publishing volume, and citation integrity from the analytics table.
Citation rate
20.48
3,915 total citations
h5-index
90
h5 depth signal
Cited share
93.5%
187 of 200
Total citations
3,915
Citation footprint
Metric signal
21.83
External metric anchor
Self-citation
2.4%
93 self-citations
Citations Trend
Monthly Publications Cadence
Citing Geographic Demographics
United States
576
China
136
United Kingdom
93
Germany
89
Canada
77
Citing Fields of Research
Neurodegenerative Disorders
848
Cell Biology
60
Neurosciences
50
Ophthalmology
36
Immunology
36
Publishing Activity & Reach
Volume, recency, access pattern, and citing-community signals from the journal analytics record.
All-time article footprint
1,611
Articles tracked across the journal lifetime
Indexed publication set
200
187 cited publications
Last 12 months
106
8.8 publications/month
Open access share
100.0%
106 OA publications in the last year
Leading citing country
United States
576 citing publications
Leading citing field
Neurodegenerative Disorders
848 citing publications
Latest tracked publication
16 October 2026
10 recent records available
Coverage & Indexing History
v6, Jan. 2011-
v1, 2006-
Active Coverage
Research Focus & Classification
Indexed Subjects
Neurodegenerative Disorders
Issuing & Sponsoring Bodies
Contributor
BioMed Central Ltd
Broad Categories
Molecular Biology
Neurology
Neurodegenerative Disorders
MeSH Descriptors
Neurobiology
Neurodegenerative Diseases
Latest Publications
Recent article records with DOI-first linking and condensed abstracts.
01
DOI 10.1186/s13024-026-01005-4
Open DOI
Disassembly of mitochondrial cristae architecture drives neurodegeneration in Huntington’s disease
Background: Mitochondrial dysfunction is a key feature of many neurodegenerative diseases, including Huntington’s disease (HD), yet the initiating cellular lesion that links the disease-causing protein, mutant huntingtin (mtHtt), to orga...
02
DOI 10.1186/s13024-026-01003-6
Open DOI
SALL1 as a marker for distinguishing microglia from blood-derived myeloid cells in stroke brain scRNA-seq data
Distinguishing resident microglia from infiltrating myeloid cells in stroke scRNA-seq data remains challenging due to shared myeloid markers; SALL1 shows greater specificity for microglia compared with commonly used markers (e.g. TMEM119...
03
DOI 10.1186/s13024-026-01006-3
Open DOI
ICA1L stabilizes LRP1 to mitigate Aβ pathology in Alzheimer’s disease
Background: Genetic and proteomic studies have identified numerous candidate genes associated with Alzheimer’s disease (AD), yet the functional relevance of many remains unclear. Islet Cell Autoantigen 1 Like (ICA1L) has consistently eme...
04
DOI 10.1186/s13024-026-00998-2
Open DOI
AI-assisted discovery of an ABCA1/ABCG1 activator for restoring mitophagy and mitigating Alzheimer’s pathology
Defective mitophagy is a key pathological risk of Alzheimer’s disease (AD), yet available pharmacological agents capable of restoring mitophagy remain clinically limited, largely due to the lack of tools for drug screening and target ide...
05
DOI 10.1186/s13024-026-01001-8
Open DOI
Nucleoporin 50 rescues hallmarks of TDP-43 proteinopathy in ALS/FTD disease models
Nuclear depletion and cytoplasmic aggregation of RNA-binding protein TDP-43 are common neuropathological hallmarks of the amyotrophic lateral sclerosis and frontotemporal degeneration (ALS/FTD) disease spectrum. Although defects in nucle...
06
DOI 10.1186/s13024-026-01002-7
Open DOI
Beneficial vs. pathogenic microglia functions across aging, multiple sclerosis, and Alzheimer’s disease
Microglia are a population of central nervous system (CNS)-resident macrophages that play key roles in regulating CNS health. Emerging work has revealed a plethora of ways by which microglia monitor and regulate neuronal and glial functi...
07
DOI 10.1186/s13024-026-00996-4
Open DOI
Oxidative stress-induced microglial CD22 upregulation impairs phagocytosis and exacerbates Huntington’s disease
Background: Huntington’s disease (HD) is a neurodegenerative disorder caused by an abnormal polyglutamine expansion in mutant huntingtin (mHTT) and is characterized by movement dysfunction and neuronal loss. Siglecs, a family of sialic a...
08
DOI 10.1186/s13024-026-01000-9
Open DOI
In vivo detection of pathologic α- synuclein and TDP-43 in the skin and olfactory mucosa of a patient with Parkinson’s disease-like phenotype carrying the p.Thr272Serfs*10 GRN mutation
We describe a patient carrying the GRN p.Thr272Serfs*10 mutation, who presented with parkinsonism at onset and later developed prodromal frontotemporal dementia, in whom seed amplification assay on olfactory mucosa and skin analyses sugg...
09
DOI 10.1186/s13024-026-00993-7
Open DOI
From mechanism to intervention: lipoproteins and Alzheimer’s disease
Alzheimer’s disease (AD) is the leading global cause of dementia, characterized by memory impairment and neuropathological hallmarks of amyloid and tau deposition. Several cardiovascular risk factors, including hypertension, type II diab...
10
DOI 10.1186/s13024-026-00997-3
Open DOI
Dynamic [18F]PI-2620 recording facilitates prediction of β-amyloid positivity and simultaneous staging of tau and neurodegeneration
Background: Patients with Alzheimer’s disease (AD) and clinically overlapping neurodegenerative diseases are classified molecularly using the A/T/N classification system. Apart from fluid biomarkers and structural MRI, A/T/N assessment i...
Bibliographical & Catalog Notes
Title from PDF caption (publisher's Web site, viewed July 19, 2006).
Latest issue consulted: 1:7 (31 July 2006) (viewed Aug. 4, 2006).
Articles added on an individual basis as accepted.
Mode of access: World Wide Web.
Mode of access: Internet.