A Comprehensive Review on the Role of the Gut Microbiome in Human Neurological Disorders DOI
Shokufeh Ghasemian Sorboni,

Hanieh Shakeri Moghaddam,

Reza Jafarzadeh Esfehani

et al.

Clinical Microbiology Reviews, Journal Year: 2022, Volume and Issue: 35(1)

Published: Jan. 5, 2022

The human body is full of an extensive number commensal microbes, consisting bacteria, viruses, and fungi, collectively termed the microbiome. initial acquisition microbiota occurs from both external maternal environments, vast majority them colonize gastrointestinal tract (GIT). These microbial communities play a central role in maturation development immune system, nervous GIT system are also responsible for essential metabolic pathways. Various factors, including host genetic predisposition, environmental lifestyle, diet, antibiotic or nonantibiotic drug use, etc., affect composition gut microbiota. Recent publications have highlighted that imbalance microflora, known as dysbiosis, associated with onset progression neurological disorders. Moreover, characterization microbiome-host cross talk pathways provides insight into novel therapeutic strategies. Novel preclinical clinical research on interventions related to microbiome treating conditions, autism spectrum disorders, Parkinson's disease, schizophrenia, multiple sclerosis, Alzheimer's epilepsy, stroke, hold significant promise. This review aims present comprehensive overview potential involvement pathogenesis particular emphasis microbe-based therapies and/or diagnostic biomarkers. discusses health benefits administration probiotics, prebiotics, postbiotics, synbiotics fecal transplantation

Language: Английский

Complement and microglia mediate early synapse loss in Alzheimer mouse models DOI Open Access
Soyon Hong,

Victoria F. Beja-Glasser,

Bianca M. Nfonoyim

et al.

Science, Journal Year: 2016, Volume and Issue: 352(6286), P. 712 - 716

Published: April 1, 2016

Too much cleaning up The complement system and microglia seek out destroy unwanted cellular debris for the peripheral immune as well excess synapses in developing brain. Hong et al. now show how may go haywire adults early progression toward Alzheimer's disease (AD). Aberrant synapse loss is an feature of correlates with cognitive decline. In mice susceptible to AD, was associated synapses, microglial function required loss. authors speculate that aberrant activation this “trash disposal” underlies AD pathology. Science , issue p. 712

Language: Английский

Citations

2643

Immune attack: the role of inflammation in Alzheimer disease DOI
Frank L. Heppner,

Richard M. Ransohoff,

Burkhard Becher

et al.

Nature reviews. Neuroscience, Journal Year: 2015, Volume and Issue: 16(6), P. 358 - 372

Published: May 20, 2015

Language: Английский

Citations

1900

Self-propagation of pathogenic protein aggregates in neurodegenerative diseases DOI
Mathias Jucker, Lary C. Walker

Nature, Journal Year: 2013, Volume and Issue: 501(7465), P. 45 - 51

Published: Sept. 3, 2013

Language: Английский

Citations

1492

The Intersection of Amyloid Beta and Tau at Synapses in Alzheimer’s Disease DOI Creative Commons
Tara L. Spires‐Jones, Bradley T. Hyman

Neuron, Journal Year: 2014, Volume and Issue: 82(4), P. 756 - 771

Published: May 1, 2014

Language: Английский

Citations

1036

Trafficking and Proteolytic Processing of APP DOI Open Access
Christian Haass, Christoph Kaether, Gopal Thinakaran

et al.

Cold Spring Harbor Perspectives in Medicine, Journal Year: 2012, Volume and Issue: 2(5), P. a006270 - a006270

Published: Feb. 7, 2012

Christian Haass1, Christoph Kaether2, Gopal Thinakaran3 and Sangram Sisodia3 DZNE—German Center for Neurodegenerative Diseases, 80336 Munich, Germany; Adolf Butenandt-Institute, Biochemistry, Ludwig-Maximilians University, Germany Leibniz Institut für Altersforschung, D-07745 Jena, Department of Neurobiology, University Chicago, Illinois 60637 Correspondence: christian.haass{at}dzne.lmu.de; ssisodia{at}bsd.uchicago.edu

Language: Английский

Citations

987

Brain Imaging in Alzheimer Disease DOI Open Access

Keith A. Johnson,

Nick C. Fox, Reisa A. Sperling

et al.

Cold Spring Harbor Perspectives in Medicine, Journal Year: 2012, Volume and Issue: 2(4), P. a006213 - a006213

Published: Jan. 31, 2012

Imaging has played a variety of roles in the study Alzheimer disease (AD) over past four decades. Initially, computed tomography (CT) and then magnetic resonance imaging (MRI) were used diagnostically to rule out other causes dementia. More recently, modalities including structural functional MRI positron emission (PET) studies cerebral metabolism with fluoro-deoxy-d-glucose (FDG) amyloid tracers such as Pittsburgh Compound-B (PiB) have shown characteristic changes brains patients AD, prodromal even presymptomatic states that can help rule-in AD pathophysiological process. No one modality serve all purposes each unique strengths weaknesses. These their particular utilities are discussed this article. The challenge for future will be combine biomarkers most efficiently facilitate diagnosis, staging, and, importantly, development effective disease-modifying therapies.

Language: Английский

Citations

794

Exercise-linked FNDC5/irisin rescues synaptic plasticity and memory defects in Alzheimer’s models DOI
Mychael V. Lourenco, Rudimar Luiz Frozza, Guilherme B. de Freitas

et al.

Nature Medicine, Journal Year: 2018, Volume and Issue: 25(1), P. 165 - 175

Published: Dec. 18, 2018

Language: Английский

Citations

744

Apolipoprotein E and Apolipoprotein E Receptors: Normal Biology and Roles in Alzheimer Disease DOI Open Access
David M. Holtzman,

Joachim Herz,

Guojun Bu

et al.

Cold Spring Harbor Perspectives in Medicine, Journal Year: 2012, Volume and Issue: 2(3), P. a006312 - a006312

Published: Jan. 10, 2012

Apolipoprotein E (APOE) genotype is the major genetic risk factor for Alzheimer disease (AD); ε4 allele increases and ε2 protective. In central nervous system (CNS), apoE produced by glial cells, present in high-density-like lipoproteins, interacts with several receptors that are members of low-density lipoprotein receptor (LDLR) family, a protein binds to amyloid-β (Aβ) peptide. There variety mechanisms which isoform may influence AD. substantial evidence differential effects on AD influenced ability affect Aβ aggregation clearance brain. Other also likely play role CNS function as well AD, including synaptic plasticity, cell signaling, lipid transport metabolism, neuroinflammation. ApoE receptors, LDLRs, Apoer2, very (VLDLRs), receptor-related 1 (LRP1) appear both metabolism toxicity. Therapeutic strategies based include influencing apoE/Aβ interactions, structure, lipidation, LDLR family member function, signaling. Understanding normal disease-related biology connecting apoE, provide novel insights into pathogenesis treatment.

Language: Английский

Citations

740

Spatial Transcriptomics and In Situ Sequencing to Study Alzheimer’s Disease DOI Creative Commons
Wei-Ting Chen,

Ashley Lu,

Katleen Craessaerts

et al.

Cell, Journal Year: 2020, Volume and Issue: 182(4), P. 976 - 991.e19

Published: July 22, 2020

Language: Английский

Citations

712

β-Amyloid accumulation in the human brain after one night of sleep deprivation DOI Creative Commons
Ehsan Shokri‐Kojori, Gene‐Jack Wang, Corinde E. Wiers

et al.

Proceedings of the National Academy of Sciences, Journal Year: 2018, Volume and Issue: 115(17), P. 4483 - 4488

Published: April 9, 2018

Significance There has been an emerging interest in sleep and its association with β-amyloid burden as a risk factor for Alzheimer’s disease. Despite the evidence that acute deprivation elevates levels mouse interstitial fluid human cerebrospinal fluid, not much is known about impact of on brain. Using positron emission tomography, here we show impacts brain regions have implicated Our observations provide preliminary negative effect

Language: Английский

Citations

700