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| 1 | Oral frailty and neurodegeneration in Alzheimer’s disease显示文摘Frailty is a critical intermediate status of the aging process with a multidimensional and multisystem nature and at higher risk for adverse health-related outcomes,including falls,disability,hospitalizations,institutionalization,mortality,dementia,and Alzheimer’s disease.Among different frailty phenotypes,oral frailty has been recently suggested as a novel construct defined as a decrease in oral function with a coexisting decline in cognitive and physical functions.We briefly reviewed existing evidence on operational definitions of oral frailty,assessment and screening tools,and possible relationships among oral frailty,oral microbiota,and Alzheimer’s disease neurodegeneration.Several underlying mechanism may explain the oral health-frailty links including undernutrition,sarcopenia linked to both poor nutrition and frailty,psychosocial factors,and the chronic inflammation typical of oral disease.Oral microbiota may influence Alzheimer’s disease risk through circulatory or neural access to the brain and the interplay with periodontal disease,often causing tooth loss also linked to an increased Alzheimer’s disease risk.On this bases,COR388,a bacterial protease inhibitor targeting Porphyromonas gingivalis implicated in periodontal disease,is now being tested in a double-blind,placebocontrolled Phase II/III study in mild-to-moderate Alzheimer’s disease.Therefore,oral status may be an important contributor to general health,including Alzheimer’s disease and latelife cognitive disorders,suggesting the central role of preventive strategies targeting the novel oral frailty phenotype and including maintenance and improvement of oral function and nutritional status to reduce the burden of both oral dysfunction and frailty. | Vittorio Dibello Madia Lozupone Daniele Manfredini Antonio Dibello Roberta Zupo Rodolfo Sardone Antonio Daniele Frank Lobbezoo Francesco Panza | 2021 | Neural Regeneration Research2021，16，11： | 10 |
| 2 | Hydroxytryptamine transporter gene-linked polymorphic region(5HTTLPR)is associated with delusions in Alzheimer’s disease显示文摘Background:Serotoninergic pathways underlying delusion symptoms in Alzheimer’s disease(AD)have not been fully clarified.5-Hydroxytryptamine transporter gene-linked polymorphic region(5-HTTLPR)is a variable number tandem repeats in the promoter region of serotonin transporter encoding-gene affecting transcription.Methods:We investigated the association of 5-HTTLPR with delusions in a total of 257 consecutive patients clinically diagnosed as AD according to the National Institute on Aging-Alzheimer’s Association criteria.All participants underwent a comprehensive evaluation with a standardized comprehensive geriatric assessment and Neuropsychiatric Inventory.Results:Delusion symptoms were observed in 171 patients(66.54%).In respect to AD patients without delusions,AD patients with delusions showed a low prevalence of S-plus carriers(5-HTTLPR-L/S+5-HTTLPR-S/S genotypes)[p<0.001;odds ratio(OR)=0.240,95% confidence interval(CI)=0.121–0.471].Logistic regression analysis adjusted for the apolipoprotein E polymorphism showed that in AD patients with delusions the presence of an 5-HTTLPR-S allele may reduce disease duration(p=0.005;OR=0.680,95% CI=0.522–0.886)and increase aberrant motor activity(p=0.013;OR=2.257,95% CI=1.195–4.260).The present findings suggested that 5-HTTLPR might be associated with delusions in AD.S-plus carriers might be associated with protective effect against delusions in AD.Conclusions:More studies on wider samples of high selected demented patients are needed to confirm our results.However,the present findings suggested that a genetic factor related to serotonin metabolism might exert a protective role on the clinical expression of neuropsychiatric clusters in AD with important implications regarding mechanisms underlying delusions and their possible treatment across the AD and dementia spectrum. | Grazia D’Onofrio Francesco Panza Daniele Sancarlo Michele Lauriola Mariangela P.Dagostino Giulia Paroni Madia Lozupone Antonio Mangiacotti Paola Bisceglia Carolina Gravina Maria Urbano Filomena Addante Francesco Paris Leandro Cascavilla Antonio Greco Davide Seripa | 2019 | Translational Neurodegeneration2019，8，1： | 2 |
| 3 | Laparoscopic treatment of simple hepatic cysts and polycystic liver disease显示文摘 | P. Fiamingo U. Tedeschi M. Veroux U. Cillo A. Brolese A. Da Rold C. Madia G. Zanus D.F. D'Amico | 2003 | Surgical Endoscopy2003，，4： | 2 |
| 4 | Serum creatinine as an index of renal function: new insights into old concepts显示文摘 | PERRONE R D MADIAS N E LEVEY A S | 1992 | Clin Chem1992，38，10： | 1 |
| 5 | Hyponatremia显示文摘 | Adrogu6 HJ Madias NE | 2000 | N Engl J Med2000，342，21： | 1 |
| 6 | Selective Catalytic Reduction of NO and NO2 at Low Temperatures 显示文摘 | Koebel M Madia G Elsener M | 2002 | Catal Today2002，73，： | 1 |
| 7 | The challenge of hyponatre- mia 显示文摘 | Adrogu6 HJ Madias NE | 2012 | J Am Soc Nephrol2012，23，7： | 1 |
| 8 | Variant angina associated with bitter orange in a dietary supplement显示文摘 | Gange C A Madias C Felix Gretzik E M | 2006 | Mayo Clinic Proc2006，81，： | 1 |
| 9 | Serum creatinine as an index of renal function: New insights into old concepts 显示文摘 | Perrone RD Madias NE Levey AS | 1992 | Clin Chem1992，38，10： | 1 |
| 10 | Primary care:hyponatremia显示文摘 | Adrogué HJ Madias NE | 2000 | N Engl J Med2000，342，： | 1 |
| 11 | Is it possible to improve survival in patients with Klnstkin tumors?显示文摘 | Veroux M Madia C Bruno G | 2003 | Tumori2003，89，4： | 1 |
| 12 | Lack of SCN1A mutationin familial seizures显示文摘 | Malacarne M Madia F Gennaro E | 2002 | Epilepsia2002，43，5： | 1 |
| 13 | Sodium and Potassium in the patho-genesis of hypertension显示文摘 | Adrogué HJ Madias NE | 2007 | N Engl J Med2007，356，： | 1 |
| 14 | Cell membrane stretch and chest blow-induced ventrieular fibrillation: commotio cordis显示文摘 | Madias C Maron B J Supron S | 2008 | J Cardiovasc Electrophysiol2008，19，12： | 1 |
| 15 | Thermal stability of vanadia - tungsta- titania catalysts in the SCR process 显示文摘 | Madia G Elsener M Koebel M | 2002 | Applied Catalysis B : Environmental2002，39，2： | 1 |
| 16 | Sodium and potassium in the patho- gensis of hypertension 显示文摘 | Adrogue H J Madias N E | 2007 | N Engl J Med2007，3，56： | 1 |
| 17 | Reaction pathways in the selective catalytic reduction process with NO and NO2 at low temperature 显示文摘 | KOEBEL M ELSENER M MADIA G | 2001 | Industrial & Engineering Chemistry Research2001，40，1： | 1 |
| 18 | Hypematremia显示文摘 | Adrogue HI Madias NE | 2000 | N Engl J Med2000，342，20： | 1 |
| 19 | Hypematremia 显示文摘 | Adrogue HJ Madias NE | 2000 | N Engl J Med2000，342，20： | 1 |
| 20 | Incidence and prevalence of hyponatremia显示文摘 | Upadhyay A J aber BL Madias NE | 2006 | Am J Med2006，119，71： | 1 |
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