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Amyloid imaging using fluorine-19 magnetic resonance imaging ((19)F-MRI)

Tooyama I, Yanagisawa D, Taguchi H, Kato T, Hirao K, Shirai N, et al.

Ageing Res Rev, 2016 09;30:85-94.
PMID: 26772439 DOI: 10.1016/j.arr.2015.12.008

The formation of senile plaques followed by the deposition of amyloid-β is the earliest pathological change in Alzheimer's disease. Thus, the detection of senile plaques remains the most important early diagnostic indicator of Alzheimer's disease. Amyloid imaging is a noninvasive technique for visualizing senile plaques in the brains of Alzheimer's patients using positron emission tomography (PET) or magnetic resonance imaging (MRI). Because fluorine-19 ((19)F) displays an intense nuclear magnetic resonance signal and is almost non-existent in the body, targets are detected with a higher signal-to-noise ratio using appropriate fluorinated contrast agents. The recent introduction of high-field MRI allows us to detect amyloid depositions in the brain of living mouse using (19)F-MRI. So far, at least three probes have been reported to detect amyloid deposition in the brain of transgenic mouse models of Alzheimer's disease; (E,E)-1-fluoro-2,5-bis-(3-hydroxycarbonyl-4-hydroxy)styrylbenzene (FSB), 1,7-bis(4'-hydroxy-3'-trifluoromethoxyphenyl)-4-methoxycarbonylethyl-1,6-heptadiene3,5-dione (FMeC1, Shiga-Y5) and 6-(3',6',9',15',18',21'-heptaoxa-23',23',23'-trifluorotricosanyloxy)-2-(4'-dimethylaminostyryl)benzoxazole (XP7, Shiga-X22). This review presents the recent advances in amyloid imaging using (19)F-MRI, including our own studies.
The influence of vitamin D supplementation on IGF-1 levels in humans: A systematic review and meta-analysis

Kord-Varkaneh H, Rinaldi G, Hekmatdoost A, Fatahi S, Tan SC, Shadnoush M, et al.

Ageing Res Rev, 2020 01;57:100996.
PMID: 31816443 DOI: 10.1016/j.arr.2019.100996

BACKGROUND: Inconsistencies exist with regard to influence of vitamin D supplementation on IGF-1 levels. The inconsistencies could be attributed to several factors, such as dosage and duration of intervention, among others. To address these inconsistencies, this study was conducted to determine the impact of vitamin D supplementation on IGF-1 levels through a systematic review and meta-analysis of randomized controlled trials (RCTs).
METHODS: A comprehensive systematic search was carried out in PubMed/MEDLINE, Web of Science, SCOPUS and Embase for RCTs that investigated the impact of vitamin D intake on circulating IGF-1 levels from inception until June 2019. Weighted mean difference (WMD) with the 95 % CI were applied for estimating combined effect size. Subgroup analysis was performed to specify the source of heterogeneity among studies.
RESULTS: Pooled results from eight studies demonstrated an overall non-significant increase in IGF-1 following vitamin D supplementation (WMD: 4 ng/ml, 95 % CI: -4 to 11). However, a significant degree of heterogeneity among studies was observed (I2 = 66 %). The subgroup analyses showed that vitamin D dosage of ≤1000 IU/day (WMD: 10 ng/ml) significantly increased IGF-1 compared to the vitamin D dosage of <1000 IU/day (WMD: -1 ng/ml). Moreover, intervention duration ≤12 weeks (WMD: 11 ng/ml) significantly increased IGF-1 compared to intervention duration <12 weeks (WMD: -3 ng/ml). In the epidemiological cohort study, participants under 60 years of age with a higher dietary vitamin D intake had significantly higher IGF-1 levels when compared to those with lower dietary vitamin D intake in second categories.
CONCLUSION: The main results indicate a non-significant increase in IGF-1 following vitamin D supplementation. Additionally, vitamin D dosages of <1000 IU/day and intervention durations of <12 weeks significantly raised IGF-1 levels.
Reply to "Double-counting of effect sizes and inappropriate exclusion of studies in "The influence of vitamin D supplementation on IGF-1 levels in humans: A systematic review and meta_analysis"

Kord-Varkaneh H, Rinaldi G, Hekmatdoost A, Fatahi S, Tan SC, Shadnoush M, et al.

Ageing Res Rev, 2021 03;66:101239.
PMID: 33346153 DOI: 10.1016/j.arr.2020.101239
Proteomics as a reliable approach for discovery of blood-based Alzheimer's disease biomarkers: A systematic review and meta-analysis

Rehiman SH, Lim SM, Neoh CF, Majeed ABA, Chin AV, Tan MP, et al.

Ageing Res Rev, 2020 07;60:101066.
PMID: 32294542 DOI: 10.1016/j.arr.2020.101066

In order to gauge the impact of proteomics in discovery of Alzheimer's disease (AD) blood-based biomarkers, this study had systematically reviewed articles published between 1984-2019. Articles that fulfilled the inclusion criteria were assessed for risk of bias. A meta-analysis was performed for replicable candidate biomarkers (CB). Of the 1651 articles that were identified, 17 case-control and two cohort studies, as well as three combined case-control and longitudinal designs were shortlisted. A total of 207 AD and mild cognitive impairment (MCI) CB were discovered, with 48 reported in >2 studies. This review highlights six CB, namely alpha-2-macroglobulin (α2M)ps, pancreatic polypeptide (PP)ps, apolipoprotein A-1 (ApoA-1)ps, afaminp, insulin growth factor binding protein-2 (IGFBP-2)ps and fibrinogen-γ-chainp, all of which exhibited consistent pattern of regulation in >three independent cohorts. They are involved in AD pathogenesis via amyloid-beta (Aβ), neurofibrillary tangles, diabetes and cardiovascular diseases (CVD). Meta-analysis indicated that ApoA-1ps was significantly downregulated in AD (SMD = -1.52, 95% CI: -1.89, -1.16, p 
Identification of blood-based biomarkers for diagnosis and prognosis of Parkinson's disease: A systematic review of proteomics studies

Chelliah SS, Bhuvanendran S, Magalingam KB, Kamarudin MNA, Radhakrishnan AK

Ageing Res Rev, 2022 01;73:101514.
PMID: 34798300 DOI: 10.1016/j.arr.2021.101514

Parkinson's Disease (PD), a neurodegenerative disorder, is characterised by the loss of motor function and dopamine neurons. Therapeutic avenues remain a challenge due to lack of accuracy in early diagnosis, monitoring of disease progression and limited therapeutic options. Proteomic platforms have been utilised to discover biomarkers for numerous diseases, a tool that may benefit the diagnosis and monitoring of disease progression in PD patients. Therefore, this systematic review focuses on analysing blood-based candidate biomarkers (CB) identified via proteomics platforms for PD. This study systematically reviewed articles across six databases (EMBASE, Cochrane, Ovid Medline, Scopus, Science Direct and PubMed) published between 2010 and 2020. Of the 504 articles identified, 12 controlled-PD studies were selected for further analysis. A total of 115 candidate biomarkers (CB) were identified across selected 12-controlled studies, of which 23 CB were found to be replicable in more than two cohorts. Using the PANTHER Go-Slim classification system and STRING network, the gene function and protein interactions between biomarkers were analysed. Our analysis highlights Apolipoprotein A-I (ApoA-I), which is essential in lipid metabolism, oxidative stress, and neuroprotection demonstrates high replicability across five cohorts with consistent downregulation across four cohorts. Since ApoA-I was highly replicable across blood fractions, proteomic platforms and continents, its relationship with cholesterol, statin and oxidative stress as PD biomarker, its role in the pathogenesis of PD is discussed in this paper. The present study identified ApoA-I as a potential biomarker via proteomics analysis of PD for the early diagnosis and prediction of disease progression.
Roles of clock genes in the pathogenesis of Parkinson's disease

Shkodina AD, Tan SC, Hasan MM, Abdelgawad M, Chopra H, Bilal M, et al.

Ageing Res Rev, 2022 02;74:101554.
PMID: 34973458 DOI: 10.1016/j.arr.2021.101554

Parkinson's disease (PD) is a common motor disorder that has become increasingly prevalent in the ageing population. Recent works have suggested that circadian rhythms disruption is a common event in PD patients. Clock genes regulate the circadian rhythm of biological processes in eukaryotic organisms, but their roles in PD remain unclear. Despite this, several lines of evidence point to the possibility that clock genes may have a significant impact on the development and progression of the disease. This review aims to consolidate recent understanding of the roles of clock genes in PD. We first summarized the findings of clock gene expression and epigenetic analyses in PD patients and animal models. We also discussed the potential contributory role of clock gene variants in the development of PD and/or its symptoms. We further reviewed the mechanisms by which clock genes affect mitochondrial dynamics as well as the rhythmic synthesis and secretion of endocrine hormones, the impairment of which may contribute to the development of PD. Finally, we discussed the limitations of the currently available studies, and suggested future potential studies to deepen our understanding of the roles of clock genes in PD pathogenesis.
Role of Sirtuin1-p53 regulatory axis in aging, cancer and cellular reprogramming

Ong ALC, Ramasamy TS

Ageing Res Rev, 2018 May;43:64-80.
PMID: 29476819 DOI: 10.1016/j.arr.2018.02.004

Regulatory role of Sirtuin 1 (SIRT1), one of the most extensively studied members of its kind in histone deacetylase family in governing multiple cellular fates, is predominantly linked to p53 activity. SIRT1 deacetylates p53 in a NAD+-dependent manner to inhibit transcription activity of p53, in turn modulate pathways that are implicated in regulation of tissue homoeostasis and many disease states. In this review, we discuss the role of SIRT1-p53 pathway and its regulatory axis in the cellular events which are implicated in cellular aging, cancer and reprogramming. It is noteworthy that these cellular events share few common regulatory pathways, including SIRT1-p53-LDHA-Myc, miR-34a,-Let7 regulatory network, which forms a positive feedback loop that controls cell cycle, metabolism, proliferation, differentiation, epigenetics and many others. In the context of aging, SIRT1 expression is reduced as a protective mechanism against oncogenesis and for maintenance of tissue homeostasis. Interestingly, its activation in aged cells is evidenced in response to DNA damage to protect the cells from p53-dependent apoptosis or senescence, predispose these cells to neoplastic transformation. Importantly, the dual roles of SIRT1-p53 axis in aging and tumourigenesis, either as tumour suppressor or tumour promoter are determined by SIRT1 localisation and type of cells. Conceptualising the distinct similarity between tumorigenesis and cellular reprogramming, this review provides a perspective discussion on involvement of SIRT1 in improving efficiency in the induction and maintenance of pluripotent state. Further research in understanding the role of SIRT1-p53 pathway and their associated regulators and strategies to manipulate this regulatory axis very likely foster the development of therapeutics and strategies for treating cancer and aging-associated degenerative diseases.
Differential gut microbiota and intestinal permeability between frail and healthy older adults: A systematic review

Rashidah NH, Lim SM, Neoh CF, Majeed ABA, Tan MP, Khor HM, et al.

Ageing Res Rev, 2022 Dec;82:101744.
PMID: 36202312 DOI: 10.1016/j.arr.2022.101744

This systematic review appraised previous findings on differential gut microbiota composition and intestinal permeability markers between frail and healthy older adults. A literature search was performed using PubMed, Scopus, ScienceDirect and the Cochrane Library. Relevant studies were shortlisted based on inclusion and exclusion criteria as well as assessed for risk of bias. The primary outcome was the differential composition of gut microbiota and/ or intestinal permeability markers between frail and healthy older adults. A total of 10 case-control studies and one cohort study were shortlisted. Based on consistent findings reported by more than one shortlisted study, the microbiota of frail older adults was characterised by decreased phylum Firmicutes, with Dialister, Lactobacillus and Ruminococcus being the prominent genera. Healthy controls, on the other hand, exhibited higher Eubacterium at the genera level. In terms of intestinal permeability, frail older adults were presented with increased serum zonulin, pro-inflammatory cytokines (TNF-α, HMGB-1, IL-6, IL1-ra, MIP-1β) and amino acids (aspartic acid and phosphoethanolamine) when compared to healthy controls. Altogether, frail elderlies had lower gut microbiota diversity and lower abundance of SCFA producers, which may have led to leaky guts, upregulated pro-inflammatory cytokines, frailty and sarcopenia.
Bio-enhanced fraction from Clitoria ternatea root extract ameliorates cognitive functions and in vivo hippocampal neuroplasticity in chronic cerebral hypoperfusion rat model

Ahad MA, Chear NJ, Keat LG, Has ATC, Murugaiyah V, Hassan Z

Ageing Res Rev, 2023 Aug;89:101990.
PMID: 37343678 DOI: 10.1016/j.arr.2023.101990

Research employing a bio-enhanced fraction of Clitoria ternatea (CT) to treat cognitive decline in the animal model has not yet been found. This study aimed to determine the neuroprotective effect of CT root bioactive fraction (CTRF) in chronic cerebral hypoperfusion (CCH) rat model. CTRF and its major compound, clitorienolactones A (CLA), were obtained using column chromatography. A validated HPLC-UV method was employed for the standardization of CTRF. CCH rats were given orally either vehicle or fraction (10, 20 and 40 mg/kg). Behavioural and hippocampal neuroplasticity studies were conducted following 4 weeks post-surgery. The brain hippocampus was extracted for proteins and neurotransmitters analyses. HPLC analysis showed that CTRF contained 25% (w/w) of CLA. All tested doses of CTRF and CLA (10 mg/kg) significantly restored cognitive deficits and reversed the inhibition of neuroplasticity by CCH. However, only CTRF (40 mg/kg) and CLA (10 mg/kg) significantly reversed the elevation of amyloid-beta plaque. Subsequently, treatment with CTRF (40 mg/kg) and CLA (10 mg/kg) alleviated the downregulation of molecular synaptic signalling proteins levels caused by CCH. The neurotransmitters level was restored following treatment of CTRF and CLA. Our finding suggested that CTRF improves memory and neuroplasticity in CCH rats which was mainly contributed by CLA.
Parkinson's disease diagnosis using deep learning: A bibliometric analysis and literature review

Abumalloh RA, Nilashi M, Samad S, Ahmadi H, Alghamdi A, Alrizq M, et al.

Ageing Res Rev, 2024 Apr;96:102285.
PMID: 38554785 DOI: 10.1016/j.arr.2024.102285

Parkinson's Disease (PD) is a progressive neurodegenerative illness triggered by decreased dopamine secretion. Deep Learning (DL) has gained substantial attention in PD diagnosis research, with an increase in the number of published papers in this discipline. PD detection using DL has presented more promising outcomes as compared with common machine learning approaches. This article aims to conduct a bibliometric analysis and a literature review focusing on the prominent developments taking place in this area. To achieve the target of the study, we retrieved and analyzed the available research papers in the Scopus database. Following that, we conducted a bibliometric analysis to inspect the structure of keywords, authors, and countries in the surveyed studies by providing visual representations of the bibliometric data using VOSviewer software. The study also provides an in-depth review of the literature focusing on different indicators of PD, deployed approaches, and performance metrics. The outcomes indicate the firm development of PD diagnosis using DL approaches over time and a large diversity of studies worldwide. Additionally, the literature review presented a research gap in DL approaches related to incremental learning, particularly in relation to big data analysis.
Effects of clitorienolactones from Clitoria ternatea root on calcium channel mediating hippocampal long-term potentiation in rats induced chronic cerebral hypoperfusion

Ahad MA, Chear NJ, Abdullah MH, Ching-Ga TAF, Liao P, Wei S, et al.

Ageing Res Rev, 2024 Apr;96:102252.
PMID: 38442748 DOI: 10.1016/j.arr.2024.102252

Chronic cerebral hypoperfusion (CCH) is a common mechanism of acute brain injury due to impairment of blood flow to the brain. Moreover, a prolonged lack of oxygen supply may result in cerebral infarction or global ischemia, which subsequently causes long-term memory impairment. Research on using Clitoria ternatea root extract for treating long-term memory has been studied extensively. However, the bioactive compound contributing to its neuroprotective effects remains uncertain. In the present study, we investigate the effects of clitorienolactone A (CLA) and B (CLB) from the roots of Clitoria ternatea extract on hippocampal neuroplasticity in rats induced by CCH. CLA and CLB were obtained using column chromatography. The rat model of CCH was induced using two-vessel occlusion surgery (2VO). The 2VO rats were given 10 mg/kg of CLA and CLB orally, followed by hippocampal neuroplasticity recording using in vivo electrophysiological. Rats received CLA and CLB (10 mg/kg) significantly reversed the impairment of long-term potentiation following 2VO surgery. Furthermore, we investigate the effect of CLA and CLB on the calcium channel using the calcium imaging technique. During hypoxia, CLA and CLB sustain the increase in intracellular calcium levels. We next predict the binding interactions of CLA and CLB against NMDA receptors containing GluN2A and GluN2B subunits using in silico molecular docking. Our result found that both CLA and CLB exhibited lower binding affinity against GluN2A and GluN2B subunits. Our findings demonstrated that bioactive compounds from Clitoria ternatea improved long-term memory deficits in the chronic cerebral hypoperfusion rat model via calcium uptake. Hence, CLA and CLB could be potential therapeutic tools for treating cognitive dysfunction.

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