Morphometric Similarity Patterning of Amyloid-β and Tau Proteins Correlates with Transcriptomics in the Alzheimer’s Disease Continuum DOI Open Access
Lorenza Brusini, G Dolci, Lorenzo Pini

и другие.

International Journal of Molecular Sciences, Год журнала: 2024, Номер 25(23), С. 12871 - 12871

Опубликована: Ноя. 29, 2024

Bridging the gap between cortical morphometric remodeling and gene expression can help to clarify effects of selective brain accumulation Amyloid-β (Aβ) tau proteins occurring in Alzheimer's disease (AD). To this aim, we derived similarity (MS) networks from 126 Aβ- tau-positive (Aβ+/tau+) 172 Aβ-/tau- subjects, investigated association group-wise regional MS differences transcriptional correlates thanks an imaging transcriptomics approach grounded Allen Human Brain Atlas (AHBA). The expressed with highest correlation alterations was

Язык: Английский

Genomic and Transcriptomic Approaches Advance the Diagnosis and Prognosis of Neurodegenerative Diseases DOI Open Access
Zheng Liu, Siyuan Song

Genes, Год журнала: 2025, Номер 16(2), С. 135 - 135

Опубликована: Янв. 24, 2025

Neurodegenerative diseases, such as Alzheimer’s disease (AD), Parkinson’s (PD), Huntington’s (HD), and amyotrophic lateral sclerosis (ALS), represent a growing societal challenge due to their irreversible progression significant impact on patients, caregivers, healthcare systems. Despite advances in clinical imaging-based diagnostics, these diseases are often detected at advanced stages, limiting the effectiveness of therapeutic interventions. Recent breakthroughs genomic transcriptomic technologies, including whole-genome sequencing, single-cell RNA sequencing (scRNA-seq), CRISPR-based screens, have revolutionized field, offering new avenues for early diagnosis personalized prognosis. Genomic approaches elucidated disease-specific genetic risk factors molecular pathways, while studies identified stage-specific biomarkers that correlate with severity. Furthermore, genome-wide association (GWAS), polygenic scores (PRS), spatial transcriptomics enabling stratification patients based profiles prognostic trajectories. Advances functional genomics uncovered actionable targets, ATXN2 ALS TREM2 AD, paving way tailored strategies. achievements, challenges remain translating discoveries into practice heterogeneity complexity neurodegenerative pathophysiology. Future integration technologies holds promise transforming diagnostic paradigms, hope improved patient outcomes precision medicine approaches.

Язык: Английский

Процитировано

2

Integrating amyloid and tau imaging with proteomics and genomics in Alzheimer’s disease DOI Creative Commons

Gabriele Vilkaite,

Jacob W. Vogel, Niklas Mattsson

и другие.

Cell Reports Medicine, Год журнала: 2024, Номер 5(9), С. 101735 - 101735

Опубликована: Сен. 1, 2024

Язык: Английский

Процитировано

8

Lipid nanoparticle (LNP) mediated mRNA delivery in neurodegenerative diseases DOI

Seyedeh Ghazal Moosavi,

Niloufar Rahiman, Mahmoud Reza Jaafari

и другие.

Journal of Controlled Release, Год журнала: 2025, Номер unknown, С. 113641 - 113641

Опубликована: Март 1, 2025

Язык: Английский

Процитировано

0

Synaptic vulnerability to amyloid-β and tau pathologies differentially disrupts emotional and memory neural circuits DOI Creative Commons
Maria Dolores Capilla-López, Ángel Deprada-Fernandez, Yuniesky Andrade‐Talavera

и другие.

Molecular Psychiatry, Год журнала: 2025, Номер unknown

Опубликована: Янв. 30, 2025

Alzheimer's disease (AD) is characterized by memory loss and neuropsychiatric symptoms associated with cerebral amyloid-β (Aβ) tau pathologies, but whether how these factors differentially disrupt neural circuits remains unclear. Here, we investigated the vulnerability of emotional to Aβ pathologies in mice expressing mutant human amyloid precursor protein (APP), Tau or both APP/Tau excitatory neurons. develop age- sex-dependent phosphorylated latter exacerbated at early stages, vulnerable brain regions. Early deficits were hippocampal pathology mice, whereas anxiety fear appeared linked intracellular basolateral amygdala (BLA) APP mice. Transcriptome profiling revealed gene changes affecting myelination RNA processing inflammation synaptic-related pathways 6 months. At 9 months, detected common region-specific astrocytic, microglia 63 AD-associated genes hippocampus BLA Spatial learning synaptic accumulation synapse disruption disturbances not BLA. Interestingly, exhibited synergistic detrimental effects long-term potentiation (LTP) they counteract each other mitigate LTP impairments amygdala. These findings indicate that cause synergize induce dysfunction immune responses, contributing differing AD.

Язык: Английский

Процитировано

0

Integration of Single-Cell and Spatial Transcriptomic Data Reveals Spatial Architecture and Potential Biomarkers in Alzheimer’s Disease DOI
Xing Fan, Huamei Li

Molecular Neurobiology, Год журнала: 2024, Номер unknown

Опубликована: Ноя. 15, 2024

Язык: Английский

Процитировано

2

Functional network disruption in cognitively unimpaired autosomal dominant Alzheimer’s disease: a magnetoencephalography study DOI Creative Commons
Anne M van Nifterick, Willem de Haan, Cornelis J. Stam

и другие.

Brain Communications, Год журнала: 2024, Номер 6(6)

Опубликована: Янв. 1, 2024

Abstract Understanding the nature and onset of neurophysiological changes, selective vulnerability central hub regions in functional network, may aid managing growing impact Alzheimer’s disease on society. However, precise alterations occurring pre-clinical stage human remain controversial. This study aims to provide increased insights quantitative during a true early disease. Using high spatial resolution source-reconstructed magnetoencephalography, we investigated regional whole-brain changes unique cohort 11 cognitively unimpaired individuals with pathogenic mutations presenilin-1 or amyloid precursor protein gene 1:3 matched control group (n = 33) median age 49 years. We examined several magnetoencephalography measures that have been shown robust detecting differences sporadic patients are sensitive excitation-inhibition imbalance. includes spectral power connectivity different frequency bands. also using disruption index. To understand how change as progresses through its stage, correlations between outcomes various clinical variables like were analysed. A comparison mutation carriers controls revealed oscillatory slowing, characterized by widespread higher theta (4–8 Hz) power, lower posterior peak occipital alpha 2 (10–13 power. Functional analyses presented (amplitude-based) (8–13 beta (13–30 bands, predominantly located parieto-temporal regions. Furthermore, found significant index for (phase-based) band, attributed both ‘non-hub’ alongside disruption. Neurophysiological did not correlate indicators progression after multiple comparisons correction. Our findings evidence slowing occur before cognitive impairment autosomal dominant leading The direction these comparable those observed stages disease, suggest an imbalance, fit activity-dependent degeneration hypothesis. These prove useful diagnosis intervention future.

Язык: Английский

Процитировано

1

Regional vulnerability to Aβ and tau pathology DOI

Lisa Kiani

Nature Reviews Neurology, Год журнала: 2024, Номер 20(3), С. 133 - 133

Опубликована: Фев. 7, 2024

Язык: Английский

Процитировано

0

How Alzheimer's Abeta propagates and triggers tau pathology in intact neurons DOI Open Access

Tomoya Sasahara,

Hongo Shoko,

Mika Ito

и другие.

bioRxiv (Cold Spring Harbor Laboratory), Год журнала: 2024, Номер unknown

Опубликована: Авг. 29, 2024

Abstract Alzheimer’s disease begins with Aβ accumulation, progresses to tau aggregates and results in widespread neurodegeneration 1-3 . Simultaneous propagation of from very limited wide distant brain regions is one the outstanding events early stage. Here, we demonstrate that neurovascular unit 4,5 comprising capillaries pericytes, machinery supplying oxygen glucose neurons, also for propagating effector molecules impose pathologies on intact neurons. We discovered two distinct signaling cascades, activated capillary endothelial cells other pericytes. At origin either cascade, identified amylospheroid (ASPD) 6,7 , a highly toxic 30-mer assembly Aβ, its sole target NKAα3 8 neuron-specific isoform Na + ,K -ATPase 9,10 but present In cells, ASPD binding releases angiotensin II, which increases β-secretase causing huge increase 42 resultant accumulation. an unknown molecule activates δ-secretase further augmenting producing pathogenic 1-368 fragment. Thus, are directly linked. Stopping cascades near by inhibiting ASPD-NKAα3 interaction may provide new therapeutic approach.

Язык: Английский

Процитировано

0

Local molecular and connectomic contributions of tau-related neurodegeneration DOI
Fardin Nabizadeh

GeroScience, Год журнала: 2024, Номер unknown

Опубликована: Сен. 30, 2024

Язык: Английский

Процитировано

0

Morphometric Similarity Patterning of Amyloid-β and Tau Proteins Correlates with Transcriptomics in the Alzheimer’s Disease Continuum DOI Open Access
Lorenza Brusini, G Dolci, Lorenzo Pini

и другие.

International Journal of Molecular Sciences, Год журнала: 2024, Номер 25(23), С. 12871 - 12871

Опубликована: Ноя. 29, 2024

Bridging the gap between cortical morphometric remodeling and gene expression can help to clarify effects of selective brain accumulation Amyloid-β (Aβ) tau proteins occurring in Alzheimer's disease (AD). To this aim, we derived similarity (MS) networks from 126 Aβ- tau-positive (Aβ+/tau+) 172 Aβ-/tau- subjects, investigated association group-wise regional MS differences transcriptional correlates thanks an imaging transcriptomics approach grounded Allen Human Brain Atlas (AHBA). The expressed with highest correlation alterations was

Язык: Английский

Процитировано

0