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Article: Therapeutics for neurodegenerative diseases by targeting the gut microbiome: from bench to bedside.

Ma, Yuan-Yuan / Li, Xin / Yu, Jin-Tai / Wang, Yan-Jiang

2024 Volume 13, Issue 1, Page(s) 12

Abstract: The aetiologies and origins of neurodegenerative diseases, such as Alzheimer's disease (AD), Parkinson's disease (PD), amyotrophic lateral sclerosis (ALS) and Huntington's disease (HD), are complex and multifaceted. A growing body of evidence suggests ... ...

Abstract	The aetiologies and origins of neurodegenerative diseases, such as Alzheimer's disease (AD), Parkinson's disease (PD), amyotrophic lateral sclerosis (ALS) and Huntington's disease (HD), are complex and multifaceted. A growing body of evidence suggests that the gut microbiome plays crucial roles in the development and progression of neurodegenerative diseases. Clinicians have come to realize that therapeutics targeting the gut microbiome have the potential to halt the progression of neurodegenerative diseases. This narrative review examines the alterations in the gut microbiome in AD, PD, ALS and HD, highlighting the close relationship between the gut microbiome and the brain in neurodegenerative diseases. Processes that mediate the gut microbiome-brain communication in neurodegenerative diseases, including the immunological, vagus nerve and circulatory pathways, are evaluated. Furthermore, we summarize potential therapeutics for neurodegenerative diseases that modify the gut microbiome and its metabolites, including diets, probiotics and prebiotics, microbial metabolites, antibacterials and faecal microbiome transplantation. Finally, current challenges and future directions are discussed.
MeSH term(s)	Humans ; Neurodegenerative Diseases/therapy ; Gastrointestinal Microbiome ; Amyotrophic Lateral Sclerosis ; Alzheimer Disease ; Parkinson Disease/therapy
Language	English
Publishing date	2024-02-27
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	2653701-1
ISSN	2047-9158
ISSN	2047-9158
DOI	10.1186/s40035-024-00404-1
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Article ; Online: TMEM106B aggregation in neurodegenerative diseases: linking genetics to function.

Jiao, Hai-Shan / Yuan, Peng / Yu, Jin-Tai

Molecular neurodegeneration

2023 Volume 18, Issue 1, Page(s) 54

Abstract: Background: Mutations of the gene TMEM106B are risk factors for diverse neurodegenerative diseases. Previous understanding of the underlying mechanism focused on the impairment of lysosome biogenesis caused by TMEM106B loss-of-function. However, ... ...

Abstract	Background: Mutations of the gene TMEM106B are risk factors for diverse neurodegenerative diseases. Previous understanding of the underlying mechanism focused on the impairment of lysosome biogenesis caused by TMEM106B loss-of-function. However, mutations in TMEM106B increase its expression level, thus the molecular process linking these mutations to the apparent disruption in TMEM106B function remains mysterious. Main body: Recent new studies reported that TMEM106B proteins form intracellular amyloid filaments which universally exist in various neurodegenerative diseases, sometimes being the dominant form of protein aggregation. In light of these new findings, in this review we systematically examined previous efforts in understanding the function of TMEM106B in physiological and pathological conditions. We propose that TMEM106B aggregations could recruit normal TMEM106B proteins and interfere with their function. Conclusions: TMEM106B mutations could lead to lysosome dysfunction by promoting the aggregation of TMEM106B and reducing these aggregations may restore lysosomal function, providing a potential therapeutic target for various neurodegenerative diseases.
MeSH term(s)	Humans ; Nerve Tissue Proteins/genetics ; Nerve Tissue Proteins/metabolism ; Neurodegenerative Diseases/genetics ; Mutation/genetics ; Membrane Proteins/genetics ; Membrane Proteins/metabolism
Chemical Substances	Nerve Tissue Proteins ; TMEM106B protein, human ; Membrane Proteins
Language	English
Publishing date	2023-08-10
Publishing country	England
Document type	Journal Article ; Review ; Research Support, Non-U.S. Gov't
ZDB-ID	2244557-2
ISSN	1750-1326 ; 1750-1326
ISSN (online)	1750-1326
ISSN	1750-1326
DOI	10.1186/s13024-023-00644-1
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Article ; Online: The causal role of circulating amino acids on neurodegenerative disorders: A two-sample Mendelian randomization study.

Cheng, Ji-Yun / Deng, Yue-Ting / Yu, Jin-Tai

Journal of neurochemistry

2023 Volume 166, Issue 6, Page(s) 972–981

Abstract: Potential associations between the risk of neurodegenerative diseases and circulating levels of amino acids have been implied in both experimental research and observational studies. However, because of the confounding and reverse causality, the findings ...

Abstract	Potential associations between the risk of neurodegenerative diseases and circulating levels of amino acids have been implied in both experimental research and observational studies. However, because of the confounding and reverse causality, the findings could be biased. We aimed to determine whether circulating amino acid levels have potential effects on the risk of neurodegenerative diseases through a more robust analysis. So, we performed a total of two MR analyses, a discovery two-sample MR analysis, and a replication test, using summary-level genome-wide association study (GWAS) data, both with circulating levels of amino acids as exposure and risk of neurodegenerative diseases as an outcome. The potential causalities between nine amino acids (Glutamine [Glu], Leucine [Leu], Isoleucine [Ile], Phenylalanine [Phe], Valine [Val], Alanine [Ala], Tyrosine [Tyr], Histidine [His], and Glycine [Gly]) and six neurodegenerative disorders (Alzheimer's disease [AD], Parkinson's disease [PD], Multiple sclerosis [MS], Frontotemporal dementia [FTD], Lewy body dementia [DLB], Amyotrophic lateral sclerosis [ALS]) were explored in this study. According to the discovery MR analysis, 1 SD. increase in circulating levels of Gln was genetically determined to result in a 13% lower risk of AD (IVW OR
MeSH term(s)	Humans ; Amino Acids/genetics ; Genome-Wide Association Study ; Mendelian Randomization Analysis ; Neurodegenerative Diseases/genetics ; Glutamine ; Parkinson Disease ; Alzheimer Disease ; Lewy Body Disease ; Causality
Chemical Substances	Amino Acids ; Glutamine (0RH81L854J)
Language	English
Publishing date	2023-08-11
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	80158-6
ISSN	1471-4159 ; 0022-3042 ; 1474-1644
ISSN (online)	1471-4159
ISSN	0022-3042 ; 1474-1644
DOI	10.1111/jnc.15937
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Article ; Online: Associations of blood cell indices and anemia with risk of incident dementia.

Qiang, Yi-Xuan / Deng, Yue-Ting / Yu, Jin-Tai

Alzheimer's & dementia : the journal of the Alzheimer's Association

2023 Volume 20, Issue 2, Page(s) 1466–1467

MeSH term(s)	Humans ; Dementia/epidemiology ; Anemia/epidemiology ; Blood Cells ; Risk Factors
Language	English
Publishing date	2023-11-27
Publishing country	United States
Document type	Letter
ZDB-ID	2211627-8
ISSN	1552-5279 ; 1552-5260
ISSN (online)	1552-5279
ISSN	1552-5260
DOI	10.1002/alz.13548
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Article: Genetic architecture of brain morphology and overlap with neuropsychiatric traits.

Ge, Yi-Jun / Fu, Yan / Gong, Weikang / Cheng, Wei / Yu, Jin-Tai

Trends in genetics : TIG

2024

Abstract: Uncovering the genetic architectures of brain morphology offers valuable insights into brain development and disease. Genetic association studies of brain morphological phenotypes have discovered thousands of loci. However, interpretation of these loci ... ...

Abstract	Uncovering the genetic architectures of brain morphology offers valuable insights into brain development and disease. Genetic association studies of brain morphological phenotypes have discovered thousands of loci. However, interpretation of these loci presents a significant challenge. One potential solution is exploring the genetic overlap between brain morphology and disorders, which can improve our understanding of their complex relationships, ultimately aiding in clinical applications. In this review, we examine current evidence on the genetic associations between brain morphology and neuropsychiatric traits. We discuss the impact of these associations on the diagnosis, prediction, and treatment of neuropsychiatric diseases, along with suggestions for future research directions.
Language	English
Publishing date	2024-05-02
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	619240-3
ISSN	1362-4555 ; 0168-9525 ; 0168-9479
ISSN (online)	1362-4555
ISSN	0168-9525 ; 0168-9479
DOI	10.1016/j.tig.2024.04.005
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Article ; Online: Prospective biomarkers of Alzheimer's disease: A systematic review and meta-analysis.

Li, Rui-Xian / Ma, Ya-Hui / Tan, Lan / Yu, Jin-Tai

Ageing research reviews

2022 Volume 81, Page(s) 101699

Abstract: Objective: Alzheimer's disease (AD) involves a series of pathological changes and some biomarkers were reported to assist in monitoring and predicting disease progression before the emergence of clinical symptoms. We aimed to identify prospective ... ...

Abstract	Objective: Alzheimer's disease (AD) involves a series of pathological changes and some biomarkers were reported to assist in monitoring and predicting disease progression before the emergence of clinical symptoms. We aimed to identify prospective biomarkers and quantify their effect on AD progression. Methods: PubMed, EMBASE and Web of Science databases were searched for prospective cohort studies published up to October 2021. Eligible studies were included, and the available data were extracted. Meta-analyses were conducted based on random-effect models. Relative risk (RR) with 95% confidence interval (CI) was adopted as the final effect size. Results: Totally 48,769 articles were identified, of which 84 studies with 20 prospective biomarkers were included in meta-analyses. In the present study, 15 biomarkers were associated with AD progression, comprising CSF Aβ42 (RR=2.49, 95%CI=1.68-3.69), t-tau (RR=1.88, 95%CI=1.49-2.37), p-tau (RR=1.74, 95%CI=1.37-2.21), tau/Aβ42 ratio (RR=5.11, 95%CI=2.01-13.00); peripheral blood Aβ42/Aβ40 (RR=1.26, 95%CI=1.05-1.51), t-tau (RR=1.33, 95%CI=1.08-1.64), NFL (RR=1.75, 95%CI=1.07-2.87); whole, left and right hippocampal volume (HV) (whole: RR=1.65, 95%CI=1.39-1.95; left: RR=2.60, 95%CI=1.02-6.64; right: RR=1.43, 95%CI=1.23-1.66), entorhinal cortex (EC) volume (RR=1.69, 95%CI=1.24-2.30), medial temporal lobe atrophy (MTA) (RR=1.52, 95%CI=1.33-1.74), 18 F-FDG PET (RR=2.24, 95%CI=1.29-3.89), 11 C-labeled Pittsburgh Compound B PET (11 C-PIB PET) (RR=3.91, 95%CI=1.06-14.41); APOE ε4 (RR=2.16, 1.83-2.55). A total of 70 articles were included in the qualitative review, in which 61 biomarkers were additionally associated with AD progression. Conclusion: CSF Aβ42, t-tau, p-tau, tau/Aβ42; peripheral blood t-tau, Aβ42/Aβ40, NFL; whole, left and right HV, EC volume, MTA, 18 F-FDG PET, 11 C-PIB PET; APOE ε4 may be promising prospective biomarkers for AD progression.
MeSH term(s)	Alzheimer Disease/complications ; Alzheimer Disease/diagnostic imaging ; Amyloid beta-Peptides ; Apolipoprotein E4 ; Atrophy ; Biomarkers ; Humans ; Prospective Studies ; tau Proteins
Chemical Substances	Amyloid beta-Peptides ; Apolipoprotein E4 ; Biomarkers ; tau Proteins
Language	English
Publishing date	2022-07-26
Publishing country	England
Document type	Journal Article ; Meta-Analysis ; Systematic Review ; Research Support, Non-U.S. Gov't
ZDB-ID	2075672-0
ISSN	1872-9649 ; 1568-1637
ISSN (online)	1872-9649
ISSN	1568-1637
DOI	10.1016/j.arr.2022.101699
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Article ; Online: Tau Toxicity in Neurodegeneration.

Liang, Shu-Yu / Wang, Zuo-Teng / Tan, Lan / Yu, Jin-Tai

Molecular neurobiology

2022 Volume 59, Issue 6, Page(s) 3617–3634

Abstract: Tau is a microtubule-associated protein widely distributed in the central nervous system (CNS). The main function of tau is to promote the assembly of microtubules and stabilize their structure. After a long period of research on neurodegenerative ... ...

Abstract	Tau is a microtubule-associated protein widely distributed in the central nervous system (CNS). The main function of tau is to promote the assembly of microtubules and stabilize their structure. After a long period of research on neurodegenerative diseases, the function and dysfunction of the microtubule-associated protein tau in neurodegenerative diseases and tau neurotoxicity have attracted increasing attention. Tauopathies are a series of progressive neurodegenerative diseases caused by pathological changes in tau, such as abnormal phosphorylation. The pathological features of tauopathies are the deposition of abnormally phosphorylated tau proteins and the aggregation of tau proteins in neurons. This article first describes the normal physiological function and dysfunction of tau proteins and then discusses the enzymes and proteins involved in tau phosphorylation and dephosphorylation, the role of tau in cell dysfunction, and the relationships between tau and several neurodegenerative diseases. The study of tau neurotoxicity provides new directions for the treatment of tauopathies.
MeSH term(s)	Humans ; Microtubules/metabolism ; Neurons/metabolism ; Phosphorylation ; Tauopathies/metabolism ; Tauopathies/pathology ; tau Proteins/metabolism ; tau Proteins/physiology
Chemical Substances	tau Proteins
Language	English
Publishing date	2022-03-31
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	645020-9
ISSN	1559-1182 ; 0893-7648
ISSN (online)	1559-1182
ISSN	0893-7648
DOI	10.1007/s12035-022-02809-3
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Article ; Online: Dementia research in 2022: advancing steadily on reflection.

Zhang, Ya-Ru / Kuo, Kevin / Dong, Qiang / Yu, Jin-Tai

The Lancet. Neurology

2022 Volume 22, Issue 1, Page(s) 10–12

MeSH term(s)	Humans ; Dementia/therapy
Language	English
Publishing date	2022-12-14
Publishing country	England
Document type	Journal Article
ZDB-ID	2081241-3
ISSN	1474-4465 ; 1474-4422
ISSN (online)	1474-4465
ISSN	1474-4422
DOI	10.1016/S1474-4422(22)00473-2
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Article ; Online: Depression in Alzheimer's Disease: Epidemiology, Mechanisms, and Treatment.

Huang, Yu-Yuan / Gan, Yi-Han / Yang, Liu / Cheng, Wei / Yu, Jin-Tai

Biological psychiatry

2023

Abstract: Depression and Alzheimer's disease (AD) are substantial public health concerns. In the past decades, a link between the 2 disease entities has received extensive acknowledgment, yet the complex nature of this relationship demands further clarification. ... ...

Abstract	Depression and Alzheimer's disease (AD) are substantial public health concerns. In the past decades, a link between the 2 disease entities has received extensive acknowledgment, yet the complex nature of this relationship demands further clarification. Some evidence indicates that midlife depression may be an AD risk factor, while a chronic course of depression in late life may be a precursor to or symptom of dementia. Recently, multiple pathophysiological mechanisms have been proposed to underlie the bidirectional relationship between depression and AD, including genetic predisposition, immune dysregulation, accumulation of AD-related biomarkers (e.g., amyloid-β and tau), and alterations in brain structure. Accordingly, numerous therapeutic approaches, such as pharmacology treatments, psychotherapy, and lifestyle interventions, have been suggested as potential means of interfering with these pathways. However, the current literature on this topic remains fragmented and lacks a comprehensive review characterizing the association between depression and AD. In this review, we aim to address these gaps by providing an overview of the co-occurrence and temporal relationship between depression and AD, as well as exploring their underlying mechanisms. We also examine the current therapeutic regimens for depression and their implications for AD management and outline key challenges facing the field.
Language	English
Publishing date	2023-10-20
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	209434-4
ISSN	1873-2402 ; 0006-3223
ISSN (online)	1873-2402
ISSN	0006-3223
DOI	10.1016/j.biopsych.2023.10.008
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Article ; Online: Associations of Growth-Associated Protein 43 with Cerebral Microbleeds: A Longitudinal Study.

Li, Da / Sun, Yan / Ding, Lin / Fu, Yan / Zhou, Jie / Yu, Jin-Tai / Tan, Lan

Journal of Alzheimer's disease : JAD

2024 Volume 97, Issue 4, Page(s) 1913–1922

Abstract: Background: Cerebral microbleeds (CMB) play an important role in neurodegenerative pathology.: Objective: The present study aims to test whether cerebrospinal fluid (CSF) growth-associated protein 43 (GAP-43) level is linked to CMBs in elderly people. ...

Abstract	Background: Cerebral microbleeds (CMB) play an important role in neurodegenerative pathology. Objective: The present study aims to test whether cerebrospinal fluid (CSF) growth-associated protein 43 (GAP-43) level is linked to CMBs in elderly people. Methods: A total of 750 participants from the Alzheimer's Disease Neuroimaging Initiative (ADNI) who had measurements of GAP-43 and CMBs were included in the study. According to the presence and extent of CMBs, participants were stratified into different groups. Regression analyses were used to assess cross-sectional and longitudinal associations between GAP-43 and CMBs. Results: Participants with CMB were slightly older and had higher concentrations of CSF GAP43. In multivariable adjusted analyses for age, gender, APOEɛ4 status, and cognitive diagnoses, higher CSF GAP-43 concentrations were modestly associated with CMB presence (OR = 1.169, 95% CI = 1.001-1.365) and number (β= 0.020, SE = 0.009, p = 0.027). Similarly, higher CSF GAP43 concentrations were accrual of CMB lesions, associated with higher CMB progression (OR = 1.231, 95% CI = 1.044-1.448) and number (β= 0.017, SE = 0.005, p = 0.001) in the follow up scan. In stratified analyses, slightly stronger associations were noted in male participants, those 65 years and older, carriers of APOEɛ4 alleles, and with more advanced cognitive disorders. Conclusions: CSF GAP-43 was cross-sectionally associated with the presence and extent of CMBs. GAP-43 might be used as a biomarker to track the dynamic changes of CMBs in elderly persons.
MeSH term(s)	Humans ; Male ; Aged ; GAP-43 Protein ; Cerebral Hemorrhage/cerebrospinal fluid ; Longitudinal Studies ; Cross-Sectional Studies ; Magnetic Resonance Imaging/methods
Chemical Substances	GAP-43 Protein
Language	English
Publishing date	2024-01-23
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	1440127-7
ISSN	1875-8908 ; 1387-2877
ISSN (online)	1875-8908
ISSN	1387-2877
DOI	10.3233/JAD-230508
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