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  1. Book: Progress in understanding moderate to severe Alzheimer disease

    Farlow, Martin R.

    (Neurology ; 65,6, Suppl. 3)

    2005  

    Author's details Martin R. Farlow, guest ed
    Series title Neurology ; 65,6, Suppl. 3
    Collection
    Language English
    Size S33 S. : graph. Darst.
    Publisher Lippincott Williams & Wilkins
    Publishing place Hagerstown, Md
    Publishing country United States
    Document type Book
    HBZ-ID HT014515496
    Database Catalogue ZB MED Medicine, Health

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    In stock of ZB MED Cologne/Königswinter

    Shelf markLoan statusLocation
    Ui II Zs 153 -65,6,Suppl.3- verfügbar in Königswinter Königswinter

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  2. Article ; Online: CAR (Current Alzheimer Research) has a ROAD (Research on AD) Even in the Lockdown.

    Lahiri, Debomoy K / Farlow, Martin R

    Current Alzheimer research

    2021  Volume 17, Issue 12, Page(s) 1053–1054

    MeSH term(s) Alzheimer Disease/drug therapy ; Biomedical Research ; COVID-19 ; Financing, Government/economics ; Humans
    Language English
    Publishing date 2021-03-11
    Publishing country United Arab Emirates
    Document type Editorial
    ZDB-ID 2205170-3
    ISSN 1875-5828 ; 1567-2050
    ISSN (online) 1875-5828
    ISSN 1567-2050
    DOI 10.2174/156720501712210222105659
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 6235: Show issues Location:
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  3. Article ; Online: Benefits and harms of atypical antipsychotics for agitation in adults with dementia.

    Farlow, Martin R / Shamliyan, Tatyana A

    European neuropsychopharmacology : the journal of the European College of Neuropsychopharmacology

    2017  Volume 27, Issue 3, Page(s) 217–231

    Abstract: We evaluated the most current evidence regarding the benefits and harms of atypical antipsychotics in adults with dementia. In June 2016, following a protocol developed a priori, we systematically searched several databases for published and unpublished ... ...

    Abstract We evaluated the most current evidence regarding the benefits and harms of atypical antipsychotics in adults with dementia. In June 2016, following a protocol developed a priori, we systematically searched several databases for published and unpublished data from randomized controlled trials (RCT), observational studies, and meta-analyses; conducted direct meta-analyses using a random effects model; and graded the quality of evidence according to the Grading of Recommendations Assessment, Development and Evaluation (GRADE) working group. One high-quality meta-analysis and published and unpublished data from 8 RCTs and 12 large observational studies met inclusion criteria. When compared with placebo, aripiprazole, risperidone, and olanzapine but not quetiapine result in modest (standardized mean difference <0.5 standard deviations) improvement in neuropsychiatric symptoms. Aripiprazole, risperidone, quetiapine, and olanzapine are associated with increased odds of acute myocardial infraction, and risperidone and olanzapine are associated with increased odds of hip fracture. Observational studies suggest no differences in all-cause mortality between atypical antipsychotics. Observational studies suggest that atypical antipsychotics are associated with lower risk of all-cause mortality and extrapyramidal symptoms but higher risk of stroke when compared with conventional antipsychotics. To manage agitation in adults with progressive dementia, clinicians may recommend atypical antipsychotics with continuous monitoring of behavioral symptoms, informing patients and their families or caregivers of the significant risk of adverse effects and baseline risk of acute myocardial infraction and bone fractures.
    MeSH term(s) Antipsychotic Agents/therapeutic use ; Dementia/complications ; Humans ; Psychiatric Status Rating Scales ; Psychomotor Agitation/drug therapy ; Psychomotor Agitation/etiology ; Treatment Outcome
    Chemical Substances Antipsychotic Agents
    Language English
    Publishing date 2017
    Publishing country Netherlands
    Document type Journal Article ; Review
    ZDB-ID 1082947-7
    ISSN 1873-7862 ; 0924-977X
    ISSN (online) 1873-7862
    ISSN 0924-977X
    DOI 10.1016/j.euroneuro.2017.01.002
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    Zs.A 3288: Show issues Location:
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    Jg. 1995 - 2021: Lesesall (2.OG)
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    Zs.MO 630: Show issues

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  4. Article ; Online: Should the ApoE genotype be a covariate for clinical trials in Alzheimer disease?

    Farlow, Martin R

    Alzheimer's research & therapy

    2010  Volume 2, Issue 3, Page(s) 15

    Abstract: Should the apolipoprotein E (ApoE) genotype be a covariate for clinical trials in Alzheimer disease (AD)? ApoE is a transport protein for lipids, amyloid-beta proteins, and the different phenotypes differentially affect amyloid-beta deposition, ... ...

    Abstract Should the apolipoprotein E (ApoE) genotype be a covariate for clinical trials in Alzheimer disease (AD)? ApoE is a transport protein for lipids, amyloid-beta proteins, and the different phenotypes differentially affect amyloid-beta deposition, neurofibrillary tangle formation, and microglial activation. The ApoE genotype has not affected efficacy in short symptomatic AD trials. ApoE4 has been associated with greater efficacy in at least two mild cognitive impairment studies. Vasogenic edema was more frequent in ApoE4 AD patients treated with a monoclonal antibody to amyloid beta. Since there is evidence that the ApoE genotype may differentially affect disease mechanisms, efficacy, and adverse effects in both AD and mild cognitive impairment trials, the ApoE genotype should be included as a covariate in future studies.
    Language English
    Publishing date 2010-06-08
    Publishing country England
    Document type Editorial
    ZDB-ID 2506521-X
    ISSN 1758-9193 ; 1758-9193
    ISSN (online) 1758-9193
    ISSN 1758-9193
    DOI 10.1186/alzrt39
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  5. Article: A Review of Dementia with Lewy Bodies' Impact, Diagnostic Criteria and Treatment.

    Capouch, Samuel D / Farlow, Martin R / Brosch, Jared R

    Neurology and therapy

    2018  Volume 7, Issue 2, Page(s) 249–263

    Abstract: Dementia with Lewy bodies is one of the most common causes of dementia. It is not as common as Alzheimer's disease; the general public's awareness of the disease is poor in comparison. Its effects on caregivers and patients alike are not well known to ... ...

    Abstract Dementia with Lewy bodies is one of the most common causes of dementia. It is not as common as Alzheimer's disease; the general public's awareness of the disease is poor in comparison. Its effects on caregivers and patients alike are not well known to the general population. There are currently no FDA-approved medications specifically for the treatment of DLB. Many of the medications that are approved for Alzheimer's disease are widely used in the treatment of DLB with varying degrees of success. Treatment of DLB is life long and requires a dedicated team of physicians and caregivers to minimize the degree of morbidity and mortality experienced by the patients suffering from the disease as it progresses.
    Language English
    Publishing date 2018-07-09
    Publishing country New Zealand
    Document type Journal Article ; Review
    ISSN 2193-8253
    ISSN 2193-8253
    DOI 10.1007/s40120-018-0104-1
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article ; Online: Measuring Subjective Cognitive Decline in Older Adults: Harmonization Between the Cognitive Change Index and the Measurement of Everyday Cognition Instruments.

    Wells, Lindsey F / Risacher, Shannon L / McDonald, Brenna C / Farlow, Martin R / Brosch, Jared / Gao, Sujuan / Apostolova, Liana G / Saykin, Andrew J

    Journal of Alzheimer's disease : JAD

    2022  Volume 87, Issue 2, Page(s) 761–769

    Abstract: Background: Self and informant (proxy or study partner) reports of everyday cognitive functioning have been shown to be associated with incipient neurodegenerative disease. The 20-item Cognitive Change Index (CCI) and the 39-item Measurement of Everyday ...

    Abstract Background: Self and informant (proxy or study partner) reports of everyday cognitive functioning have been shown to be associated with incipient neurodegenerative disease. The 20-item Cognitive Change Index (CCI) and the 39-item Measurement of Everyday Cognition (ECog) were each developed to characterize early subjective changes in cognitive function.
    Objective: We examined the relationship between CCI and ECog self and informant-based evaluations to determine content overlap and provide a co-calibration for converting between these widely used instruments.
    Methods: 950 participants (57.1% female, mean age = 71.2 years) from ADNI and the Indiana ADRC with self-based evaluations and 279 participants (60.9% female, mean age = 71.8 years) with informant-based evaluations (Indiana ADRC) were included. Analyzed variables for the CCI and ECog included domain mean scores, memory domain total scores, and total scores for all items. Spearman correlations, regression analyses, and frequency distributions were used to assess the relationship between CCI and ECog. Sex, age, years of education, race/ethnicity, APOE ɛ4 carrier status, and baseline diagnosis were also analyzed as potentially relevant covariates.
    Results: CCI and ECog total scores were highly correlated for the self (r = 0.795, p < 0.001) and informant-based (r = 0.840, p < 0.001) versions, as expected. Frequency distributions of self and informant total scores were generated and plotted separately. Quadratic regressions for self (r2 = 0.626) and informant (r2 = 0.741) scores were used to create a translation table between the CCI and ECog total scores.
    Conclusion: Self and informant total scores can be harmonized and translated between the CCI and ECog to facilitate cross-study and longitudinal assessment of perceived cognitive change, an important patient-reported outcome.
    MeSH term(s) Aged ; Cognition ; Cognitive Dysfunction/psychology ; Diagnostic Self Evaluation ; Ethnicity ; Female ; Humans ; Male ; Neurodegenerative Diseases ; Neuropsychological Tests
    Language English
    Publishing date 2022-03-30
    Publishing country Netherlands
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
    ZDB-ID 1440127-7
    ISSN 1875-8908 ; 1387-2877
    ISSN (online) 1875-8908
    ISSN 1387-2877
    DOI 10.3233/JAD-215388
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 6084: Show issues Location:
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  7. Article: The SERAD study of the safety and efficacy of galantamine in severe Alzheimer's disease.

    Farlow, Martin R

    The Lancet. Neurology

    2009  Volume 8, Issue 1, Page(s) 22–23

    MeSH term(s) Activities of Daily Living ; Aged ; Aged, 80 and over ; Alzheimer Disease/drug therapy ; Clinical Trials as Topic ; Galantamine/adverse effects ; Galantamine/therapeutic use ; Humans ; Nootropic Agents/adverse effects ; Nootropic Agents/therapeutic use ; Randomized Controlled Trials as Topic
    Chemical Substances Nootropic Agents ; Galantamine (0D3Q044KCA)
    Language English
    Publishing date 2009-01
    Publishing country England
    Document type Comment ; Letter ; Research Support, Non-U.S. Gov't
    ZDB-ID 2081241-3
    ISSN 1474-4422
    ISSN 1474-4422
    DOI 10.1016/S1474-4422(08)70262-X
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 5955: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (2.OG)
    ab Jg. 2022: Lesesaal (EG)

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  8. Article ; Online: Spatial transcriptomic patterns underlying amyloid-β and tau pathology are associated with cognitive dysfunction in Alzheimer's disease.

    Yu, Meichen / Risacher, Shannon L / Nho, Kwangsik T / Wen, Qiuting / Oblak, Adrian L / Unverzagt, Frederick W / Apostolova, Liana G / Farlow, Martin R / Brosch, Jared R / Clark, David G / Wang, Sophia / Deardorff, Rachael / Wu, Yu-Chien / Gao, Sujuan / Sporns, Olaf / Saykin, Andrew J

    Cell reports

    2024  Volume 43, Issue 2, Page(s) 113691

    Abstract: Amyloid-β (Aβ) and tau proteins accumulate within distinct neuronal systems in Alzheimer's disease (AD). Although it is not clear why certain brain regions are more vulnerable to Aβ and tau pathologies than others, gene expression may play a role. We ... ...

    Abstract Amyloid-β (Aβ) and tau proteins accumulate within distinct neuronal systems in Alzheimer's disease (AD). Although it is not clear why certain brain regions are more vulnerable to Aβ and tau pathologies than others, gene expression may play a role. We study the association between brain-wide gene expression profiles and regional vulnerability to Aβ (gene-to-Aβ associations) and tau (gene-to-tau associations) pathologies by leveraging two large independent AD cohorts. We identify AD susceptibility genes and gene modules in a gene co-expression network with expression profiles specifically related to regional vulnerability to Aβ and tau pathologies in AD. In addition, we identify distinct biochemical pathways associated with the gene-to-Aβ and the gene-to-tau associations. These findings may explain the discordance between regional Aβ and tau pathologies. Finally, we propose an analytic framework, linking the identified gene-to-pathology associations to cognitive dysfunction in AD at the individual level, suggesting potential clinical implication of the gene-to-pathology associations.
    MeSH term(s) Humans ; Transcriptome/genetics ; Alzheimer Disease/genetics ; Gene Expression Profiling ; Amyloid beta-Peptides ; Cognitive Dysfunction/genetics
    Chemical Substances Amyloid beta-Peptides
    Language English
    Publishing date 2024-01-19
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2649101-1
    ISSN 2211-1247 ; 2211-1247
    ISSN (online) 2211-1247
    ISSN 2211-1247
    DOI 10.1016/j.celrep.2024.113691
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  9. Article: A multicenter, randomized, double-blind, placebo-controlled ascending dose study to evaluate the safety, tolerability, pharmacokinetics (PK) and pharmacodynamic (PD) effects of Posiphen in subjects with Early Alzheimer's Disease.

    Galasko, Douglas / Farlow, Martin R / Lucey, Brendan P / Honig, Lawrence S / Elbert, Donald / Bateman, Randall / Momper, Jeremiah / Thomas, Ronald / Rissman, Robert A / Pa, Judy / Aslanyan, Vahan / Balasubramanian, Archana / West, Tim / Maccecchini, Maria / Feldman, Howard H

    medRxiv : the preprint server for health sciences

    2024  

    Abstract: Background: Amyloid beta protein (Aβ) is a treatment target in Alzheimer's Disease (AD). Lowering production of its parent protein, APP, has benefits in preclinical models. Posiphen binds to an iron-responsive element in APP mRNA and decreases ... ...

    Abstract Background: Amyloid beta protein (Aβ) is a treatment target in Alzheimer's Disease (AD). Lowering production of its parent protein, APP, has benefits in preclinical models. Posiphen binds to an iron-responsive element in APP mRNA and decreases translation of APP and Aβ. To augment human data for Posiphen, we evaluated safety, tolerability and pharmacokinetic and pharmacodynamic (PD) effects on Aβ metabolism using Stable Isotope Labeling Kinetic (SILK) analysis.
    Methods: Double-blind phase 1b randomized ascending dose clinical trial, at five sites, under an IRB-approved protocol. Participants with mild cognitive impairment or mild AD (Early AD) with positive CSF biomarkers were randomized (within each dose arm) to Posiphen or placebo. Pretreatment assessment included lumbar puncture for CSF. Participants took Posiphen or placebo for 21-23 days, then underwent CSF catheter placement, intravenous infusion of
    Results: From June 2017 to December 2021, 19 participants were enrolled, in dose cohorts (6 active: 2 placebo) of 60 mg once/day and 60 mg twice/day; 1 participant was enrolled and completed 60 mg three times/day. 10 active drug and 5 placebo participants completed all study procedures. Posiphen was safe and well-tolerated. 8 participants had headaches related to CSF catheterization; 5 needed blood patches. Prespecified SILK analyses of Fractional Synthesis Rate (FSR) for CSF Aβ40 showed no significant overall or dose-dependent effects of Posiphen vs. placebo. Comprehensive multiparameter modeling of APP kinetics supported dose-dependent lowering of APP production by Posiphen. Cognitive measures and CSF biomarkers did not change significantly from baseline to 21 days in Posiphen vs placebo groups.
    Conclusions: Posiphen was safe and well-tolerated in Early AD. A multicenter SILK study was feasible. Findings are limited by small sample size but provide additional supportive safety and PK data. Comprehensive modeling of biomarker dynamics using SILK data may reveal subtle drug effects.
    Trial registration: NCT02925650 on clinicaltrials.gov.
    Language English
    Publishing date 2024-03-22
    Publishing country United States
    Document type Preprint
    DOI 10.1101/2024.03.20.24304638
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  10. Article ; Online: Randomized clinical trial results for donepezil in Alzheimer's disease: is the treatment glass half full or half empty?

    Farlow, Martin R

    Journal of the American Geriatrics Society

    2008  Volume 56, Issue 8, Page(s) 1566–1567

    MeSH term(s) Activities of Daily Living ; Advertising as Topic ; Aged ; Alzheimer Disease/drug therapy ; Conflict of Interest ; Double-Blind Method ; Drug Industry/economics ; Economic Competition ; Evidence-Based Medicine ; Humans ; Indans/adverse effects ; Indans/economics ; Indans/therapeutic use ; Marketing ; Nootropic Agents/adverse effects ; Nootropic Agents/economics ; Nootropic Agents/therapeutic use ; Piperidines/adverse effects ; Piperidines/economics ; Piperidines/therapeutic use ; Randomized Controlled Trials as Topic ; Treatment Outcome
    Chemical Substances Indans ; Nootropic Agents ; Piperidines ; donepezil (8SSC91326P)
    Language English
    Publishing date 2008-08
    Publishing country United States
    Document type Comment ; Journal Article
    ZDB-ID 80363-7
    ISSN 1532-5415 ; 0002-8614
    ISSN (online) 1532-5415
    ISSN 0002-8614
    DOI 10.1111/j.1532-5415.2008.01853.x
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