Latest & greatest articles for alzheimer

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Alzheimer’s disease

Alzheimer’s disease is a chronic neurodegenerative disease responsible for the majority of cases of dementia. This progressive disease disrupts memory and thinking due to an accumulation of plaques and tangles in the brain. As the disease progresses, these get progressively worse.

What causes Alzheimer’s diseases is poorly understood, although there is a strong genetic component which could account for the majority (~70%) of the risk. Other risk factors have been identified, such as depression, head injuries and hypertension. Alzheimer’s disease is typically a disease of older people.

Although Alzheimer’s disease cannot currently be cured but it can be managed. With cholinesterase inhibitors being a common intervention as well as memantine (an NMDA receptor antagonist) and psychosocial interventions.

Trip has an extensive collection of research evidence and articles relating to Alzheimer’s disease including clinical guidelines, systematic reviews, synopses, clinical trials and case reports.

Top results for alzheimer

41. CSF tau and the CSF tau/ABeta ratio for the diagnosis of Alzheimer's disease dementia and other dementias in people with mild cognitive impairment (MCI).

CSF tau and the CSF tau/ABeta ratio for the diagnosis of Alzheimer's disease dementia and other dementias in people with mild cognitive impairment (MCI). BACKGROUND: Research suggests that measurable change in cerebrospinal fluid (CSF) biomarkers occurs years in advance of the onset of clinical symptoms (Beckett 2010). In this review, we aimed to assess the ability of CSF tau biomarkers (t-tau and p-tau) and the CSF tau (t-tau or p-tau)/ABeta ratio to enable the detection of Alzheimer's disease (...) pathology in patients with mild cognitive impairment (MCI). These biomarkers have been proposed as important in new criteria for Alzheimer's disease dementia that incorporate biomarker abnormalities. OBJECTIVES: To determine the diagnostic accuracy of 1) CSF t-tau, 2) CSF p-tau, 3) the CSF t-tau/ABeta ratio and 4) the CSF p-tau/ABeta ratio index tests for detecting people with MCI at baseline who would clinically convert to Alzheimer's disease dementia or other forms of dementia at follow-up. SEARCH

Cochrane2017

42. Pharmacological aspects of galantamine for the treatment of Alzheimer's disease

Pharmacological aspects of galantamine for the treatment of Alzheimer's disease 28337117 2018 11 13 1611-2156 16 2017 EXCLI journal EXCLI J Pharmacological aspects of galantamine for the treatment of Alzheimer's disease. 35-39 10.17179/excli2016-820 Kim Jae Kwang JK Division of Life Sciences, College of Life Sciences and Bioengineering, Incheon National University, Incheon, 406-772, Korea. Park Sang Un SU Department of Crop Science, Chungnam National University, 99 Daehak-ro, Yuseong-gu (...) , Daejeon, 34134, Korea. eng Journal Article 2017 01 10 Germany EXCLI J 101299402 1611-2156 2016 12 04 2017 01 04 2017 3 25 6 0 2017 3 25 6 0 2017 3 25 6 1 epublish 28337117 10.17179/excli2016-820 2016-820 Doc35 PMC5318685 Bioorg Med Chem. 2015 Sep 1;23(17):5382-9 26260334 Mater Sci Eng C Mater Biol Appl. 2016 Aug 1;65:151-63 27157738 J Ethnopharmacol. 2004 Jun;92(2-3):147-62 15137996 Molecules. 2016 Jan 11;21(1):53 26760993 Alzheimers Res Ther. 2014 Jul 21;6(4):47 25478019 Drug Deliv. 2016 Oct;23 (8

EXCLI journal2017 Full Text: Link to full Text with Trip Pro

44. Interventions to Prevent Age-Related Cognitive Decline, Mild Cognitive Impairment, and Clinical Alzheimer's-Type Dementia

Interventions to Prevent Age-Related Cognitive Decline, Mild Cognitive Impairment, and Clinical Alzheimer's-Type Dementia Comparative Effectiveness Review Number 188 Interventions To Prevent Age-Related Cognitive Decline, Mild Cognitive Impairment, and Clinical Alzheimer’s-Type Dementia eComparative Effectiveness Review Number 188 Interventions To Prevent Age-Related Cognitive Decline, Mild Cognitive Impairment, and Clinical Alzheimer’s-Type Dementia Prepared for: Agency for Healthcare Research (...) @ahrq.hhs.gov. Suggested citation: Kane RL, Butler M, Fink HA, Brasure M, Davila H, Desai P, Jutkowitz E, McCreedy E, Nelson VA, McCarten JR, Calvert C, Ratner E, Hemmy LS, Barclay T. Interventions To Prevent Age-Related Cognitive Decline, Mild Cognitive Impairment, and Clinical Alzheimer’s-Type Dementia. Comparative Effectiveness Review No. 188. (Prepared by the Minnesota Evidence-based Practice Center under Contract No. 290-2015-00008-I.) AHRQ Publication No. 17-EHC008-EF. Rockville, MD: Agency

Effective Health Care Program (AHRQ)2017

45. Targeting Functional Decline in Alzheimer Disease: A Randomized Trial.

Targeting Functional Decline in Alzheimer Disease: A Randomized Trial. Background: Alzheimer disease results in progressive functional decline, leading to loss of independence. Objective: To determine whether collaborative care plus 2 years of home-based occupational therapy delays functional decline. Design: Randomized, controlled clinical trial. (ClinicalTrials.gov: NCT01314950 ). Setting: Urban public health system. Patients: 180 community-dwelling participants with Alzheimer disease (...) and their informal caregivers. Intervention: All participants received collaborative care for dementia. Patients in the intervention group also received in-home occupational therapy delivered in 24 sessions over 2 years. Measurements: The primary outcome measure was the Alzheimer's Disease Cooperative Study Group Activities of Daily Living Scale (ADCS ADL); performance-based measures included the Short Physical Performance Battery (SPPB) and Short Portable Sarcopenia Measure (SPSM). Results: At baseline

Annals of Internal Medicine2016 Full Text: Link to full Text with Trip Pro

46. Efficacy and safety of tau-aggregation inhibitor therapy in patients with mild or moderate Alzheimer's disease: a randomised, controlled, double-blind, parallel-arm, phase 3 trial.

Efficacy and safety of tau-aggregation inhibitor therapy in patients with mild or moderate Alzheimer's disease: a randomised, controlled, double-blind, parallel-arm, phase 3 trial. BACKGROUND: Leuco-methylthioninium bis(hydromethanesulfonate; LMTM), a stable reduced form of the methylthioninium moiety, acts as a selective inhibitor of tau protein aggregation both in vitro and in transgenic mouse models. Methylthioninium chloride has previously shown potential efficacy as monotherapy in patients (...) with Alzheimer's disease. We aimed to determine whether LMTM was safe and effective in modifying disease progression in patients with mild to moderate Alzheimer's disease. METHODS: We did a 15-month, randomised, controlled double-blind, parallel-group trial at 115 academic centres and private research clinics in 16 countries in Europe, North America, Asia, and Russia with patients younger than 90 years with mild to moderate Alzheimer's disease. Patients concomitantly using other medicines for Alzheimer's

Lancet2016 Full Text: Link to full Text with Trip Pro

47. Treatment of epilepsy for people with Alzheimer's disease.

Treatment of epilepsy for people with Alzheimer's disease. BACKGROUND: Any type of seizure can be observed in Alzheimer's disease (AD). Antiepileptic drugs seem to prevent the recurrence of epileptic seizures in most people with AD. There are pharmacological and non-pharmacological treatments for epilepsy in people with AD. There are no current systematic reviews to evaluate the efficacy and tolerability of the treatment. This review aims to review those different modalities. OBJECTIVES (...) : To assess the efficacy and tolerability of the treatment of epilepsy for people with Alzheimer's disease (AD) (including sporadic AD and dominantly inherited AD). SEARCH METHODS: We searched the Cochrane Epilepsy Group Specialized Register (1 February 2016), the Cochrane Central Register of Controlled Trials (1 February 2016), MEDLINE (Ovid, 1 February 2016) and ClinicalTrials.gov (1 February 2016). In an effort to identify further published, unpublished and ongoing trials, we searched ongoing trials

Cochrane2016

48. Positron Emission Tomography (PET) for Alzheimer disease

Positron Emission Tomography (PET) for Alzheimer disease Positron Emission Tomography (PET) for Alzheimer disease Positron Emission Tomography (PET) for Alzheimer disease HAYES, Inc. Record Status This is a bibliographic record of a published health technology assessment. No evaluation of the quality of this assessment has been made for the HTA database. Citation HAYES, Inc.. Positron Emission Tomography (PET) for Alzheimer disease. Lansdale: HAYES, Inc.. Directory Publication. 2016 Authors (...) ' conclusions Purpose of Technology: Positron emission tomography (PET) is a 3-dimensional (3D) nuclear imaging technique that measures the level of physiologic and biochemical activity or other organic function in an organ or tissue by reflecting the distribution of a radiotracer that has been administered to the patient. PET has been proposed as a method for diagnosing and predicting development of Alzheimer disease (AD). Relevant Questions: Is PET an accurate diagnostic test for detection or prediction

Health Technology Assessment (HTA) Database.2016

49. Persistent infections, immune-senescence and Alzheimer's disease

Persistent infections, immune-senescence and Alzheimer's disease 27489858 2016 08 04 2018 11 13 2331-4737 3 5-6 2016 Oncoscience Oncoscience Persistent infections, immune-senescence and Alzheimer's disease. 135-42 10.18632/oncoscience.309 Alzheimer's disease (AD) is a progressive neurodegenerative disorder and the most common cause of dementia. Classical hallmarks of AD such as amyloid deposition and neurofibrillary tangles do not completely explain AD pathogenesis. Recent investigations (...) . Porcellini Elisa E Department of Experimental, Diagnostic and Specialty Medicine, School of Medicine, University of Bologna, Bologna 40126, Italy. eng News 2016 06 30 United States Oncoscience 101636666 2331-4737 Scand J Infect Dis. 2000;32(3):237-48 10879592 Nat Genet. 2011 May;43(5):436-41 21460841 J Alzheimers Dis. 2015;48(2):319-53 26401998 Mol Neurobiol. 2014 Oct;50(2):534-44 24567119 J Alzheimers Dis. 2014;42(4):1239-50 25024328 J Pathol. 2002 Jul;197(3):395-402 12115887 J Alzheimers Dis. 2015;43(3

Oncoscience2016 Full Text: Link to full Text with Trip Pro

50. Distributions of susceptibility loci to late onset Alzheimer's disease on human chromosomes

Distributions of susceptibility loci to late onset Alzheimer's disease on human chromosomes 27540352 2016 08 19 2018 11 13 1611-2156 15 2016 EXCLI journal EXCLI J Distributions of susceptibility loci to late onset Alzheimer's disease on human chromosomes. 403-5 10.17179/excli2016-161 Saadat Mostafa M Department of Biology, College of Sciences, Shiraz University, Shiraz 71467-13565, Iran. eng Journal Article 2016 06 22 Germany EXCLI J 101299402 1611-2156 Cytogenet Cell Genet. 1993;63(3):147-50

EXCLI journal2016 Full Text: Link to full Text with Trip Pro

51. Heterogeneity of Treatment Response to Citalopram for Patients With Alzheimer`s Disease With Aggression or Agitation: The CitAD Randomized Clinical Trial

Heterogeneity of Treatment Response to Citalopram for Patients With Alzheimer`s Disease With Aggression or Agitation: The CitAD Randomized Clinical Trial 26771737 2016 05 02 2017 05 09 2017 05 09 1535-7228 173 5 2016 May 01 The American journal of psychiatry Am J Psychiatry Heterogeneity of Treatment Response to Citalopram for Patients With Alzheimer's Disease With Aggression or Agitation: The CitAD Randomized Clinical Trial. 465-72 10.1176/appi.ajp.2015.15050648 Pharmacological treatments (...) for agitation and aggression in patients with Alzheimer's disease have shown limited efficacy. The authors assessed the heterogeneity of response to citalopram in the Citalopram for Agitation in Alzheimer Disease (CitAD) study to identify individuals who may be helped or harmed. In this double-blind parallel-group multicenter trial of 186 patients with Alzheimer's disease and clinically significant agitation, participants were randomly assigned to receive citalopram or placebo for 9 weeks, with the dosage

EvidenceUpdates2016

52. Alzheimer's disease.

Alzheimer's disease. Although the prevalence of dementia continues to increase worldwide, incidence in the western world might have decreased as a result of better vascular care and improved brain health. Alzheimer's disease, the most prevalent cause of dementia, is still defined by the combined presence of amyloid and tau, but researchers are gradually moving away from the simple assumption of linear causality as proposed in the original amyloid hypothesis. Age-related, protective, and disease (...) -promoting factors probably interact with the core mechanisms of the disease. Amyloid β42, and tau proteins are established core cerebrospinal biomarkers; novel candidate biomarkers include amyloid β oligomers and synaptic markers. MRI and fluorodeoxyglucose PET are established imaging techniques for diagnosis of Alzheimer's disease. Amyloid PET is gaining traction in the clinical arena, but validity and cost-effectiveness remain to be established. Tau PET might offer new insights and be of great help

Lancet2016

53. Disclosing Pleiotropic Effects During Genetic Risk Assessment for Alzheimer Disease: A Randomized, Controlled Trial.

Disclosing Pleiotropic Effects During Genetic Risk Assessment for Alzheimer Disease: A Randomized, Controlled Trial. 26810768 2016 02 02 2016 06 13 2017 02 20 1539-3704 164 3 2016 Feb 02 Annals of internal medicine Ann. Intern. Med. Disclosing Pleiotropic Effects During Genetic Risk Assessment for Alzheimer Disease: A Randomized Trial. 155-63 10.7326/M15-0187 Increasing use of genetic testing raises questions about disclosing secondary findings, including pleiotropic information. To determine (...) the safety and behavioral effect of disclosing modest associations between apolipoprotein E (APOE) genotype and coronary artery disease (CAD) risk during APOE-based genetic risk assessments for Alzheimer disease (AD). Randomized, multicenter equivalence clinical trial. (ClinicalTrials.gov: NCT00462917). 4 teaching hospitals. 257 asymptomatic adults were enrolled, 69% of whom had 1 AD-affected first-degree relative. Disclosure of genetic risk information about AD and CAD (AD+CAD) or AD only (AD-only

Annals of Internal Medicine2016 Full Text: Link to full Text with Trip Pro

54. Amyloid‐Beta Positron Emission Tomography Imaging of Alzheimer's Pathology in Parkinson's Disease Dementia

Amyloid‐Beta Positron Emission Tomography Imaging of Alzheimer's Pathology in Parkinson's Disease Dementia 27500181 2018 11 13 2330-1619 3 4 2016 Jul-Aug Movement disorders clinical practice Mov Disord Clin Pract Amyloid-Beta Positron Emission Tomography Imaging of Alzheimer's Pathology in Parkinson's Disease Dementia. 367-375 Neuronal loss and α-synuclein (α-syn) pathology are diagnostic of PD in the appropriate clinical context. However, some PD patients have co-morbid Alzheimer's disease (...) States Journal Article 2016 01 05 United States Mov Disord Clin Pract 101630279 2330-1619 Neuroimaging autopsy neurodegeneration parkinsonism tauopathy 2016 8 9 6 0 2016 8 9 6 0 2016 8 9 6 0 ppublish 27500181 10.1002/mdc3.12290 PMC4971540 NIHMS729430 J Neurol Neurosurg Psychiatry. 1992 Mar;55(3):181-4 1564476 J Nucl Med. 2013 Jan;54(1):70-7 23166389 Sci Aging Knowledge Environ. 2006 Mar 08;2006(6):re1 16525193 J Neuropathol Exp Neurol. 2014 Jan;73(1):72-80 24335535 Alzheimers Dement. 2014 Jul;10(4

Movement disorders clinical practice2016 Full Text: Link to full Text with Trip Pro

55. Pharmacological interventions: Lack of clinically useful response predictors for treating aggression and agitation in Alzheimer's disease with citalopram

Pharmacological interventions: Lack of clinically useful response predictors for treating aggression and agitation in Alzheimer's disease with citalopram Lack of clinically useful response predictors for treating aggression and agitation in Alzheimer's disease with citalopram | Evidence-Based Mental Health This site uses cookies. By continuing to browse the site you are agreeing to our use of cookies. Log in using your username and password For personal accounts OR managers of institutional (...) accounts Username * Password * your user name or password? Search for this keyword Search for this keyword Main menu Log in using your username and password For personal accounts OR managers of institutional accounts Username * Password * your user name or password? You are here Lack of clinically useful response predictors for treating aggression and agitation in Alzheimer's disease with citalopram Article Text Further commentaries Electronic pages Pharmacological interventions Lack of clinically

Evidence-Based Mental Health2016

56. [Detection and diagnosis of Alzheimer's disease and other neurocognitive disorders]

[Detection and diagnosis of Alzheimer's disease and other neurocognitive disorders] Repérage et processus menant au diagnostic de la maladie d'Alzheimer et d'autres troubles neurocognitifs [Detection and diagnosis of Alzheimer's disease and other neurocognitive disorders] Repérage et processus menant au diagnostic de la maladie d'Alzheimer et d'autres troubles neurocognitifs [Detection and diagnosis of Alzheimer's disease and other neurocognitive disorders] Collette C, Robitaille G Record (...) Status This is a bibliographic record of a published health technology assessment from a member of INAHTA. No evaluation of the quality of this assessment has been made for the HTA database. Citation Collette C, Robitaille G. Repérage et processus menant au diagnostic de la maladie d'Alzheimer et d'autres troubles neurocognitifs. [Detection and diagnosis of Alzheimer's disease and other neurocognitive disorders] Quebec: Institut national d'excellence en sante et en services sociaux (INESSS). 2015

Health Technology Assessment (HTA) Database.2016

57. Pioglitazone and Alzheimers Disease, a Possible Treatment and Preventative Modality

Pioglitazone and Alzheimers Disease, a Possible Treatment and Preventative Modality "Pioglitazone and Alzheimers Disease, a Possible Treatment and Preventa" by Jeffrey C. Otis < > > > > > Title Author Date of Award Summer 8-8-2016 Degree Type Capstone Project Degree Name Master of Science in Physician Assistant Studies Rights . Abstract Background : Alzheimers disease is common and debilitating, and diabetes is a widely documented risk factor for the development of Alzheimers disease. Given (...) that Alzheimers disease and diabetes are two extremely common and comorbid conditions in geriatric populations that greatly affect quality of life, it follows that treatment and prevention of both pathologies be exhaustively investigated. This is especially evident, as there is no existing medication that prevents or reverses the pathogenesis of Alzheimers disease. Pioglitazone, a peroxisome proliferator-activated receptor gamma agonists of the thiazolidinedione drug class, acts by up-regulating gene

Pacific University EBM Capstone Project2016

58. Randomised controlled trial: Dextromethorphan and quinidine are suitable for off-label short-term treatment of agitation in people with Alzheimer's disease following first-line non-drug approaches

Randomised controlled trial: Dextromethorphan and quinidine are suitable for off-label short-term treatment of agitation in people with Alzheimer's disease following first-line non-drug approaches Dextromethorphan and quinidine are suitable for off-label short-term treatment of agitation in people with Alzheimer's disease following first-line non-drug approaches | Evidence-Based Medicine This site uses cookies. By continuing to browse the site you are agreeing to our use of cookies. Log (...) in using your username and password For personal accounts OR managers of institutional accounts Username * Password * your user name or password? Search for this keyword Search for this keyword Main menu Log in using your username and password For personal accounts OR managers of institutional accounts Username * Password * your user name or password? You are here Dextromethorphan and quinidine are suitable for off-label short-term treatment of agitation in people with Alzheimer's disease following

Evidence-Based Medicine (Requires free registration)2016

59. Alterations in dorsal and ventral posterior cingulate connectivity in APOE ε4 carriers at risk of Alzheimer's disease

Alterations in dorsal and ventral posterior cingulate connectivity in APOE ε4 carriers at risk of Alzheimer's disease 27703739 2018 11 13 2056-4724 1 2 2015 Oct BJPsych open BJPsych Open Alterations in dorsal and ventral posterior cingulate connectivity in APOE ε 4 carriers at risk of Alzheimer's disease. 139-148 Recent evidence suggests that exercise plays a role in cognition and that the posterior cingulate cortex (PCC) can be divided into dorsal and ventral subregions based on distinct (...) , GE Healthcare, Piramal and Navidea for amyloid imaging. C.S. has provided clinical consultancy and been on scientific advisory committees for the Australian CSIRO, Alzheimer's Australia, University of Melbourne and other relationships, which are subject to confidentiality clauses; she has been a named Chief Investigator on investigator-driven collaborative research projects in partnership with Pfizer, Merck, Piramal, Bayer and GE Healthcare. Her research programme has received support from

BJPsych open2015 Full Text: Link to full Text with Trip Pro

60. Montreal Cognitive Assessment for the diagnosis of Alzheimer's disease and other dementias.

Montreal Cognitive Assessment for the diagnosis of Alzheimer's disease and other dementias. BACKGROUND: Dementia is a progressive syndrome of global cognitive impairment with significant health and social care costs. Global prevalence is projected to increase, particularly in resource-limited settings. Recent policy changes in Western countries to increase detection mandates a careful examination of the diagnostic accuracy of neuropsychological tests for dementia. OBJECTIVES: To determine

Cochrane2015