Nature Search

Midkine attenuates amyloid-β fibril assembly and plaque formation

Zaman, Yang and Huang et al. demonstrate MDK’s suppressive effect on amyloid-β and its impact on amyloid burden and microglial activation in Alzheimer disease mice, highlighting its protective role in pathogenesis.

Masihuz Zaman
Shu Yang
Junmin Peng
Research21 Aug 2025
Nature Structural & Molecular Biology

P: 1-11
Two-step detection of Lewy body pathology via smell-function testing and CSF α-synuclein seed amplification

CSF α-synuclein seed amplification assays detect Lewy body pathology accurately but are invasive and costly. Here, the authors show that a two-step workflow using smell-function prescreening maintained 94% accuracy while reducing CSF testing by 43%.

Sophie E. Mastenbroek
Lyduine E. Collij
Oskar Hansson
ResearchOpen Access05 Aug 2025
Nature Communications

Volume: 16, P: 1-9
Tau PET positivity in individuals with and without cognitive impairment varies with age, amyloid-β status, APOE genotype and sex

Ossenkoppele, Coomans and colleagues analyzed the tau PET data of 12,048 individuals from 42 cohorts worldwide. They found that age, amyloid-β status, presence of an APOE ε4 allele and female sex are key contributors to tau PET positivity, which should aid clinical decision-making and trial designs.

Rik Ossenkoppele
Emma M. Coomans
Oskar Hansson
ResearchOpen Access16 Jul 2025
Nature Neuroscience

Volume: 28, P: 1610-1621
Deciphering distinct genetic risk factors for FTLD-TDP pathological subtypes via whole-genome sequencing

Here the authors identify TNIP1 as a risk factor for a fatal neurodegenerative disorder and discover specific genetic loci associated with the three main subtypes of this disorder. The findings highlight distinct disease mechanisms, emphasizing the roles of immunity and the notch signaling pathway.

Cyril Pottier
Fahri Küçükali
Rosa Rademakers
ResearchOpen Access25 Apr 2025
Nature Communications

Volume: 16, P: 1-19
GRAMD1B is a regulator of lipid homeostasis, autophagic flux and phosphorylated tau

The relationship between lipid dyshomeostasis and tau pathology in FTLD and AD remains unclear. Here, the authors demonstrate that GRAMD1B contributes to lipid dyshomeostasis, autophagy impairment, and tau hyperphosphorylation in neurons.

Diana Acosta Ingram
Emir Turkes
Hongjun Fu
ResearchOpen Access09 Apr 2025
Nature Communications

Volume: 16, P: 1-24
Spatial proteomics of Alzheimer’s disease-specific human microglial states

In this Resource paper, the authors use MIBI spatial proteomics to map microglial cell states in brains from cognitively normal humans and those with Alzheimer’s disease.

Dunja Mrdjen
Bryan J. Cannon
Sean C. Bendall
Research22 Jul 2025
Nature Immunology

Volume: 26, P: 1397-1410
Disease progression modelling reveals heterogeneity in trajectories of Lewy-type α-synuclein pathology

Lewy body diseases exhibit notable clinical and pathological heterogeneity. Here, the authors found three distinct trajectories of Lewy body pathology that are associated with different clinicopathological characteristics.

Sophie E. Mastenbroek
Jacob W. Vogel
Oskar Hansson
ResearchOpen Access15 Jun 2024
Nature Communications

Volume: 15, P: 1-15
Circular RNAs in the human brain are tailored to neuron identity and neuropsychiatric disease

Dopamine neurons control movements while pyramidal neurons regulate memory and language. Here the authors show that circular RNAs production in these neurons appears tailored to neuron identity and genetically linked to neuropsychiatric disease such as Parkinson’s and Alzheimer’s disease.

Xianjun Dong
Yunfei Bai
Clemens R. Scherzer
ResearchOpen Access18 Sept 2023
Nature Communications

Volume: 14, P: 1-12
TREM1 disrupts myeloid bioenergetics and cognitive function in aging and Alzheimer disease mouse models

The role of TREM1 in neurodegenerative diseases is unclear. Here the authors show that TREM1 promotes cognitive decline in aging and in the context of amyloid pathology in a mouse model of Alzheimer disease.

Edward N. Wilson
Congcong Wang
Katrin I. Andreasson
Research27 Mar 2024
Nature Neuroscience

Volume: 27, P: 873-885
APOE4/4 is linked to damaging lipid droplets in Alzheimer’s disease microglia

A microglial state, featuring lipid droplets and secretion of neurotoxic factors, is shown to be most prominent in people with Alzheimer’s disease who have the APOE4 genotype.

Michael S. Haney
Róbert Pálovics
Tony Wyss-Coray
ResearchOpen Access13 Mar 2024
Nature

Volume: 628, P: 154-161
Single cell transcriptomes and multiscale networks from persons with and without Alzheimer’s disease

Multi-omic profiling of matched brain and peripheral tissues offer rare opportunities to uncover extra-CNS drivers of Alzheimer’s pathobiology. Here, authors report an Alzheimer’s linked CD83(+) microglia subtype that is associated with immunoglobulin IgG4 production in the transverse colon.

Qi Wang
Jerry Antone
Benjamin P. Readhead
ResearchOpen Access10 Jul 2024
Nature Communications

Volume: 15, P: 1-16
CXCR6 orchestrates brain CD8⁺ T cell residency and limits mouse Alzheimer’s disease pathology

Chi and colleagues identify brain-resident CXCR6⁺PD-1⁺CD8⁺ T cells that interact with resident microglia to limit immune-mediated pathology in a mouse model of Alzheimer’s disease.

Wei Su
Jordy Saravia
Hongbo Chi
Research07 Sept 2023
Nature Immunology

Volume: 24, P: 1735-1747
Genome sequencing analysis identifies new loci associated with Lewy body dementia and provides insights into its genetic architecture

Whole-genome sequence analysis identifies five independent risk loci for Lewy body dementia and demonstrates overlapping genetic architecture with Alzheimer’s and Parkinson’s diseases.

Ruth Chia
Marya S. Sabir
Sonja W. Scholz
Research15 Feb 2021
Nature Genetics

Volume: 53, P: 294-303
Author Correction: Elucidating causative gene variants in hereditary Parkinson’s disease in the Global Parkinson’s Genetics Program (GP2)

Lara M. Lange
Micol Avenali
Masharip Atadzhanov
Amendments and CorrectionsOpen Access13 Sept 2023
npj Parkinson's Disease

Volume: 9, P: 1-3
Alzheimer’s disease-associated U1 snRNP splicing dysfunction causes neuronal hyperexcitability and cognitive impairment

Splicing dysfunction has been observed in Alzheimer’s disease but it remains unclear whether splicing defects have a causal role. Here the authors generate a mouse model with perturbed U1 snRNP activity, recapitulating RNA splicing defects, neuron hyperexcitability, neurodegeneration and synergy with the amyloid cascade when crossed with 5xFAD mice.

Ping-Chung Chen
Xian Han
Junmin Peng
Research12 Oct 2022
Nature Aging

Volume: 2, P: 923-940
Large-scale proteomic analysis of human brain identifies proteins associated with cognitive trajectory in advanced age

Cognitive abilities tend to decline over time in advanced age, yet some individuals experience stable abilities or rapid decline. Here the authors present a proteome-wide association study of cognitive trajectory, and identify 38 proteins associated with cognitive resilience.

Aliza P. Wingo
Eric B. Dammer
Thomas S. Wingo
ResearchOpen Access08 Apr 2019
Nature Communications

Volume: 10, P: 1-14
Plasma P-tau181 in Alzheimer’s disease: relationship to other biomarkers, differential diagnosis, neuropathology and longitudinal progression to Alzheimer’s dementia

Plasma P-tau18 level increased with progression of Alzheimer’s disease (AD) and differentiated AD dementia from other neurodegenerative diseases, supporting its further development as a blood-based biomarker for AD.

Shorena Janelidze
Niklas Mattsson
Oskar Hansson
Research02 Mar 2020
Nature Medicine

Volume: 26, P: 379-386
A cross-disease resource of living human microglia identifies disease-enriched subsets and tool compounds recapitulating microglial states

Profiling >200,000 live human microglia from 74 donors across neurological diseases reveals 12 subtypes of microglia that were validated in situ. Camptothecin is also identified as a compound reducing disease-enriched microglial subsets.

John F. Tuddenham
Mariko Taga
Philip L. De Jager
Research15 Oct 2024
Nature Neuroscience

Volume: 27, P: 2521-2537
Large-scale deep multi-layer analysis of Alzheimer’s disease brain reveals strong proteomic disease-related changes not observed at the RNA level

The authors analyzed the levels of more than 8,600 proteins across more than 1,000 brain tissues to arrive at a consensus AD brain protein co-expression network that illustrates the complexity and multiple pathological processes that occur in AD, many of which are not reflected at the RNA level.

Erik C. B. Johnson
E. Kathleen Carter
Nicholas T. Seyfried
ResearchOpen Access03 Feb 2022
Nature Neuroscience

Volume: 25, P: 213-225
Multi-ancestry genome-wide association meta-analysis of Parkinson’s disease

Multi-ancestry genome-wide association analyses identify new risk loci for Parkinson’s disease, and fine-mapping and co-localization analyses implicate candidate genes whose expression is associated with disease susceptibility.

Jonggeol Jeffrey Kim
Dan Vitale
Ignacio Mata
ResearchOpen Access28 Dec 2023
Nature Genetics

Volume: 56, P: 27-36
A same day α-synuclein RT-QuIC seed amplification assay for synucleinopathy biospecimens

Sabiha Parveen
Parvez Alam
Byron Caughey
ResearchOpen Access11 Feb 2025
npj Biosensing

Volume: 2, P: 1-9
Insights into ancestral diversity in Parkinson’s disease risk: a comparative assessment of polygenic risk scores

Paula Saffie-Awad
Spencer M. Grant
Sara Bandres-Ciga
ResearchOpen Access03 Jul 2025
npj Parkinson's Disease

Volume: 11, P: 1-13
Common mitochondrial deletions in RNA-Seq: evaluation of bulk, single-cell, and spatial transcriptomic datasets

A methods application study demonstrates that the Splice-Break2 pipeline can detect large mitochondrial DNA deletions in RNA-Seq data. Analyses includes GTEx and GEO datasets and demonstrate differences across tissues, brain regions, and age.

Audrey A. Omidsalar
Carmel G. McCullough
Brooke E. Hjelm
ResearchOpen Access17 Feb 2024
Communications Biology

Volume: 7, P: 1-20
Towards early diagnosis and screening of Alzheimer’s disease using frequency locked whispering gallery mode microtoroids

Adley Gin
Phuong-Diem Nguyen
Judith Su
ResearchOpen Access28 Aug 2024
npj Biosensing

Volume: 1, P: 1-9
Pharmacophore modelling based virtual screening and molecular dynamics identified the novel inhibitors and drug targets against Waddlia chondrophila

Sidra Aslam
Hossam M. Aljawdah
Geidy E. Serrano
ResearchOpen Access12 Jun 2024
Scientific Reports

Volume: 14, P: 1-15
Differential methylation analysis in neuropathologically confirmed dementia with Lewy bodies

An epigenome-wide association study of dementia with Lewy bodies discovers differentially methylated probes, genomic regions and pathways associated with this disease.

Paolo Reho
Sara Saez-Atienzar
Sonja W. Scholz
ResearchOpen Access05 Jan 2024
Communications Biology

Volume: 7, P: 1-10
The LRRK2 p.L1795F variant causes Parkinson’s disease in the European population

Lara M. Lange
Kristin Levine
Masharip Atadzhanov
ResearchOpen Access25 Mar 2025
npj Parkinson's Disease

Volume: 11, P: 1-10
Accumulation of multiple neurodegenerative disease-related proteins in familial frontotemporal lobar degeneration associated with granulin mutation

Masato Hosokawa
Hiromi Kondo
Tetsuaki Arai
ResearchOpen Access04 May 2017
Scientific Reports

Volume: 7, P: 1-11
Application of new biologic disease criteria for synucleinopathies to the systemic synuclein sampling study cohort

We applied biologic criteria and NSD-ISS to Synuclein Sampling Study, a PD sample with range of durations since clinical diagnosis. 93% of evaluable participants met biologic criteria. The majority were NSD-ISS stage3 or less, including >40% of the advanced PD group. Interpretation of staging in medicated patients is challenging. Biologic criteria and clinico-biomarker staging are important steps forward, but quantitative biomarkers of disease progression, not influenced by medications, are critically needed.

L. M. Chahine
M. C. Brumm
Charles L. White III
Comments & OpinionOpen Access06 Apr 2025
npj Parkinson's Disease

Volume: 11, P: 1-3
Defining the causes of sporadic Parkinson’s disease in the global Parkinson’s genetics program (GP2)

Clodagh Towns
Madeleine Richer
Masharip Atadzhanov
ResearchOpen Access12 Sept 2023
npj Parkinson's Disease

Volume: 9, P: 1-6

Search

Midkine attenuates amyloid-β fibril assembly and plaque formation

Two-step detection of Lewy body pathology via smell-function testing and CSF α-synuclein seed amplification

Tau PET positivity in individuals with and without cognitive impairment varies with age, amyloid-β status, APOE genotype and sex

Deciphering distinct genetic risk factors for FTLD-TDP pathological subtypes via whole-genome sequencing

GRAMD1B is a regulator of lipid homeostasis, autophagic flux and phosphorylated tau

Spatial proteomics of Alzheimer’s disease-specific human microglial states

Disease progression modelling reveals heterogeneity in trajectories of Lewy-type α-synuclein pathology

Circular RNAs in the human brain are tailored to neuron identity and neuropsychiatric disease

TREM1 disrupts myeloid bioenergetics and cognitive function in aging and Alzheimer disease mouse models

APOE4/4 is linked to damaging lipid droplets in Alzheimer’s disease microglia

Single cell transcriptomes and multiscale networks from persons with and without Alzheimer’s disease

CXCR6 orchestrates brain CD8⁺ T cell residency and limits mouse Alzheimer’s disease pathology

Genome sequencing analysis identifies new loci associated with Lewy body dementia and provides insights into its genetic architecture

Author Correction: Elucidating causative gene variants in hereditary Parkinson’s disease in the Global Parkinson’s Genetics Program (GP2)

Alzheimer’s disease-associated U1 snRNP splicing dysfunction causes neuronal hyperexcitability and cognitive impairment

Large-scale proteomic analysis of human brain identifies proteins associated with cognitive trajectory in advanced age

Plasma P-tau181 in Alzheimer’s disease: relationship to other biomarkers, differential diagnosis, neuropathology and longitudinal progression to Alzheimer’s dementia

A cross-disease resource of living human microglia identifies disease-enriched subsets and tool compounds recapitulating microglial states

Large-scale deep multi-layer analysis of Alzheimer’s disease brain reveals strong proteomic disease-related changes not observed at the RNA level

Multi-ancestry genome-wide association meta-analysis of Parkinson’s disease

A same day α-synuclein RT-QuIC seed amplification assay for synucleinopathy biospecimens

Insights into ancestral diversity in Parkinson’s disease risk: a comparative assessment of polygenic risk scores

Common mitochondrial deletions in RNA-Seq: evaluation of bulk, single-cell, and spatial transcriptomic datasets

Towards early diagnosis and screening of Alzheimer’s disease using frequency locked whispering gallery mode microtoroids

Pharmacophore modelling based virtual screening and molecular dynamics identified the novel inhibitors and drug targets against Waddlia chondrophila

Differential methylation analysis in neuropathologically confirmed dementia with Lewy bodies

The LRRK2 p.L1795F variant causes Parkinson’s disease in the European population

Accumulation of multiple neurodegenerative disease-related proteins in familial frontotemporal lobar degeneration associated with granulin mutation

Application of new biologic disease criteria for synucleinopathies to the systemic synuclein sampling study cohort

Defining the causes of sporadic Parkinson’s disease in the global Parkinson’s genetics program (GP2)

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