Relation between Uric Acid and Alzheimer's Disease in Elderly Jordanians

Al-Khateeb, Eman M.; Althaher, Arwa R.; Al-Khateeb, Mohammed S.; Al-Musawi, Hanan; Azzouqah, Ola; Al-Shweiki, Samir; Shafagoj, Yanal

doi:10.3233/jad-142037

Cited by 44 publications

(32 citation statements)

References 40 publications

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“…Uric acid in the PD model considerably attenuated the disease [139]. A study in AD patients also showed protective role of uric acid [140]. Exogenous administration of uric acid is also neuroprotective in experimental models of CNS diseases such as brain ischemia, meningitis, and ischemic stroke [138].…”

Section: Damage-associated Molecular Patternsmentioning

confidence: 99%

Sterile Neuroinflammation and Strategies for Therapeutic Intervention

Banjara

Ghosh

2017

International Journal of Inflammation

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Sterile neuroinflammation is essential for the proper brain development and tissue repair. However, uncontrolled neuroinflammation plays a major role in the pathogenesis of various disease processes. The endogenous intracellular molecules so called damage-associated molecular patterns or alarmins or damage signals that are released by activated or necrotic cells are thought to play a crucial role in initiating an immune response. Sterile inflammatory response that occurs in Alzheimer's disease (AD), Parkinson's disease (PD), stroke, hemorrhage, epilepsy, or traumatic brain injury (TBI) creates a vicious cycle of unrestrained inflammation, driving progressive neurodegeneration. Neuroinflammation is a key mechanism in the progression (e.g., AD and PD) or secondary injury development (e.g., stroke, hemorrhage, stress, and TBI) of multiple brain conditions. Hence, it provides an opportunity for the therapeutic intervention to prevent progressive tissue damage and loss of function. The key for developing anti-neuroinflammatory treatment is to minimize the detrimental and neurotoxic effects of inflammation while promoting the beneficial and neurotropic effects, thereby creating ideal conditions for regeneration and repair. This review outlines how inflammation is involved in the pathogenesis of major nonpathogenic neuroinflammatory conditions and discusses the complex response of glial cells to damage signals. In addition, emerging experimental anti-neuroinflammatory drug treatment strategies are discussed.

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Section: Damage-associated Molecular Patternsmentioning

confidence: 99%

Sterile Neuroinflammation and Strategies for Therapeutic Intervention

Banjara

Ghosh

2017

International Journal of Inflammation

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“…Of the remaining 35 studies, 6 studies were excluded for irrelevant outcomes and 5 studies were excluded for no usable data. Thus, 24 studies were finally included into the meta-analysis [14][15][16][17][18][19][20][21][22][23][24][28][29][30][31][32][33][34][35][36][37][38][39][40]. Among those 24 studies, 21 were case-control studies comparing serum uric acid levels in Alzheimer's disease patients with healthy controls [14-24, 28-32, 36-40] and 3 studies were cohort studies assessing risk of Alzheimer's disease in individuals with various categories of serum uric acid levels [33][34][35].…”

Section: Characteristics Of Included Studiesmentioning

confidence: 99%

“…Among those 24 studies, 21 were case-control studies comparing serum uric acid levels in Alzheimer's disease patients with healthy controls [14-24, 28-32, 36-40] and 3 studies were cohort studies assessing risk of Alzheimer's disease in individuals with various categories of serum uric acid levels [33][34][35]. Among those 24 studies, 19 studies were published in English [14][15][16][17][18][19][20][21][22][23][24][28][29][30][31][32][33][34][35] while the other 5 studies were published in Chinese [36][37][38][39][40]. Those 21 case-control studies included a total of 1128 cases of Alzheimer's disease and 2498 controls without Alzheimer's disease [14-24, 28-32, 36-40].…”

Section: Characteristics Of Included Studiesmentioning

confidence: 99%

“…Considering the protective effect of uric acid on nerves, the association between Alzheimer's disease and uric acid levels had gained great interest in recent years [14][15][16][17][18][19][20][21][22][23][24]. There were a number of studies performed to assess the association between Alzheimer's disease and uric acid levels, but no definite evidence was available [14][15][16][17][18][19][20][21][22][23][24]. We thus performed a systematic review and meta-analysis of relevant studies to comprehensively estimate the association.…”

Section: Introductionmentioning

confidence: 99%

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Inverse Association Between Serum Uric Acid Levels and Alzheimer’s Disease Risk

Hou

et al. 2015

Mol Neurobiol

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The association between Alzheimer's disease and uric acid levels had gained great interest in recent years, but there was still lack of definite evidence. A systematic review and meta-analysis of relevant studies was performed to comprehensively estimate the association. Relevant studies published before October 26, 2014, were searched in PubMed, Embase, and China Biology Medicine (CBM) databases. Study-specific data were combined using random-effects or fixed-effects models of meta-analysis according to between-study heterogeneity. Twenty-four studies (21 case-control and 3 cohort studies) were finally included into the meta-analysis. Those 21 case-control studies included a total of 1128 cases of Alzheimer's disease and 2498 controls without Alzheimer's disease. Those 3 cohort studies included a total of 7327 participants. Meta-analysis showed that patients with Alzheimer's disease had lower levels of uric acid than healthy controls (weighted mean difference (WMD) = -0.77 mg/dl, 95% CI -2.28 to -0.36, P = 0.0002). High serum uric acid levels were significantly associated with decreased risk of Alzheimer's disease (risk ratio (RR) = 0.66, 95% CI 0.52-0.85, P = 0.001). There was low risk of publication bias in the meta-analysis. There is an inverse association between serum uric acid levels and Alzheimer's disease. High serum uric acid level is a protective factor of Alzheimer's disease.

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“…In addition, serum uric acid (UA) levels might be decreased in patients with Alzheimer's disease and Parkinsonism dementia (McFarland et al 2013;Al-khateeb et al 2015). A published meta-analysis in 2016 has reported a significant relationship between lower serum level of UA and development of Alzheimer's disease and Parkinsonism dementia (Khan et al 2016).…”

Section: Introductionmentioning

confidence: 99%

Long-Term Subclinical Hyperglycemia and Hypoglycemia as Independent Risk Factors for Mild Cognitive Impairment in Elderly People

Wang

Zhao

Han

et al. 2017

Tohoku J. Exp. Med.

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Dementia is one of the most common geriatric diseases, and mild cognitive impairment (MCI) is considered to be incipient dementia. MCI patients have elevated risk of progressing to dementia. Multiple metabolic abnormalities have an unconfirmed effect on MCI risk, and taking adequate measures against metabolic abnormalities might prevent the developing of MCI. Thus, the present study explored the association of MCI risk with common metabolic abnormalities, such as hyperglycemia, hypoglycemia, hyperlipidemia and hypouricemia, and to provide the basis for MCI prevention. A total of 1,262 elderly outpatients with normal cognitive function and without confirmed diabetes mellitus, hyperlipoidemia and gout were enrolled. During the five-year follow-up period, 142 subjects were diagnosed with MCI according to Mini Mental State Examination and Montreal Cognitive Assessment. Furthermore, annual blood glucose, glycated hemoglobin, lipids and uric acid values were obtained, and mean of each indicator was calculated. Only mean values were included in the study to reflect long-term effect of metabolic abnormalities on MCI risk. Thus, the increased risk of MCI was associated with the mean values of blood glucose < 4.7 mmol/L (RR: 1.57, 95% CI: 1.14-2.32), blood glucose ≥ 6.3 mmol/L (RR: 1.49, 95% CI: 1.03-2.39), glycated hemoglobin ≥ 5.9% (RR: 2.28, 95% CI: 1.59-3.91), triglycerides ≥ 2.0 mmol/L (RR: 2.79, 95% CI: 2.14-3.79), total cholesterol ≥ 5.5 mmol/L (RR: 2.37, 95% CI: 1.69-3.39) and uric acid ≤ 380 μmol/L (RR: 1.62, 95% CI: 1.08-2.51). In conclusion, long-term subclinical hyperglycemia, hypoglycemia, hyperlipidemia, and hypouricemia are independent risk factors for MCI in elderly people.

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Relation between Uric Acid and Alzheimer's Disease in Elderly Jordanians

Abstract: The results suggest that serum UA levels are significantly lower in AD patients in comparison to control subjects. UA may have a protective role against AD; however this role needs further investigations.

Cited by 44 publications

References 40 publications

Sterile Neuroinflammation and Strategies for Therapeutic Intervention

Sterile Neuroinflammation and Strategies for Therapeutic Intervention

Inverse Association Between Serum Uric Acid Levels and Alzheimer’s Disease Risk

Long-Term Subclinical Hyperglycemia and Hypoglycemia as Independent Risk Factors for Mild Cognitive Impairment in Elderly People

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