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dihydroxyphenylalanine and Acute Confusional Senile Dementia

dihydroxyphenylalanine has been researched along with Acute Confusional Senile Dementia in 14 studies

Dihydroxyphenylalanine: A beta-hydroxylated derivative of phenylalanine. The D-form of dihydroxyphenylalanine has less physiologic activity than the L-form and is commonly used experimentally to determine whether the pharmacological effects of LEVODOPA are stereospecific.
dopa : A hydroxyphenylalanine carrying hydroxy substituents at positions 3 and 4 of the benzene ring.

Research Excerpts

ExcerptRelevanceReference
"For example, in substantia nigra in Parkinson's diseases key alterations occur, in iron handling, mitochondrial function and antioxidant defences, particularly reduced glutathione."2.39Oxidative stress in Parkinson's disease and other neurodegenerative disorders. ( Jenner, P, 1996)
"The selective VTA DAergic neuron degeneration results in lower DA outflow in the hippocampus and nucleus accumbens (NAc) shell."1.46Dopamine neuronal loss contributes to memory and reward dysfunction in a model of Alzheimer's disease. ( Aversa, D; Berretta, N; Cavallucci, V; Coccurello, R; Cordella, A; Cutuli, D; D'Amelio, M; De Bartolo, P; Dell'Acqua, MC; Federici, M; Giacovazzo, G; Keller, F; Krashia, P; Latagliata, EC; Marino, R; Mercuri, NB; Nobili, A; Petrosini, L; Puglisi-Allegra, S; Rizzo, FR; Sancandi, M; Viscomi, MT, 2017)
"21 patients who had Parkinson's disease (PD), PD plus dementia of Alzheimer type (PDAT) or progressive supranuclear palsy (PSP), were studied with positron emission tomography (PET) using (18F)-2-fluoro-2-deoxy-D-glucose (FDG)."1.28Positron emission tomography in degenerative disorders of the dopaminergic system. ( Heiss, WD; Herholz, K; Holthoff, V; Huber, M; Karbe, H; Wagner, R; Wienhard, K, 1992)
"Patients with Parkinson's disease have a decrement in homovanillic acid that is reversed by treatment with L-3,4-dihydroxyphenylalanine."1.27Monoamine metabolites in human cerebrospinal fluid. HPLC/ED method. ( Aguado, EG; de Yebenes, JG; Mena, MA, 1984)

Research

Studies (14)

TimeframeStudies, this research(%)All Research%
pre-19902 (14.29)18.7374
1990's7 (50.00)18.2507
2000's1 (7.14)29.6817
2010's3 (21.43)24.3611
2020's1 (7.14)2.80

Authors

AuthorsStudies
Pineda-Pardo, JA1
Gasca-Salas, C1
Fernández-Rodríguez, B1
Rodríguez-Rojas, R1
Del Álamo, M1
Obeso, I1
Hernández-Fernández, F1
Trompeta, C1
Martínez-Fernández, R1
Matarazzo, M1
Mata-Marín, D1
Guida, P1
Duque, A1
Albillo, D1
Plaza de Las Heras, I1
Montero, JI1
Foffani, G1
Toltsis, G1
Rachmilevitch, I1
Blesa, J1
Obeso, JA1
Nobili, A1
Latagliata, EC1
Viscomi, MT1
Cavallucci, V1
Cutuli, D1
Giacovazzo, G1
Krashia, P1
Rizzo, FR1
Marino, R1
Federici, M1
De Bartolo, P1
Aversa, D1
Dell'Acqua, MC1
Cordella, A1
Sancandi, M1
Keller, F1
Petrosini, L1
Puglisi-Allegra, S1
Mercuri, NB1
Coccurello, R1
Berretta, N1
D'Amelio, M1
Tsunoda, T1
Takase, M1
Shigemori, H1
Veronese, M1
Moro, L1
Arcolin, M1
Dipasquale, O1
Rizzo, G1
Expert, P1
Khan, W1
Fisher, PM1
Svarer, C1
Bertoldo, A1
Howes, O1
Turkheimer, FE1
Li, J1
Zhu, M1
Manning-Bog, AB1
Di Monte, DA1
Fink, AL1
Mena, MA1
Aguado, EG1
de Yebenes, JG1
Itoh, M2
Meguro, K2
Fujiwara, T2
Hatazawa, J1
Iwata, R1
Ishiwata, K1
Takahashi, T1
Ido, T1
Sasaki, H1
Jenner, P1
Yamaguchi, S1
Yamadori, A1
Raskind, MA1
Peskind, ER1
Holmes, C1
Goldstein, DS2
Karbe, H1
Holthoff, V1
Huber, M1
Herholz, K1
Wienhard, K1
Wagner, R1
Heiss, WD1
Barker, R1
Liu, HC1
Yang, JC1
Chang, YF1
Liu, TY1
Chi, CW1
Eisenhofer, G1
Stull, R1
Keiser, HR1
Sunderland, T1
Murphy, DL1
Kopin, IJ1

Clinical Trials (3)

Trial Overview

TrialPhaseEnrollmentStudy TypeStart DateStatus
A Study to Evaluate the Safety and Feasibility of Temporary Blood Brain Barrier Disruption (BBBD) Using Exablate MR Guided Focused Ultrasound in Patients With Parkinson's Disease Dementia[NCT03608553]10 participants (Anticipated)Interventional2018-11-26Active, not recruiting
Prazosin for Disruptive Agitation in Alzheimer's Disease (AD) (PEACE-AD)[NCT03710642]Phase 235 participants (Actual)Interventional2018-10-23Completed
Reference Values for Plasma Catechols[NCT00267904]Phase 146 participants (Actual)Interventional2006-03-08Completed
[information is prepared from clinicaltrials.gov, extracted Sep-2024]

Trial Outcomes

ADCS-ADL-Severe

"The ADCS-ADL-Severe questionnaire is a secondary outcome measure aimed at detecting functional decline in people with severe AD. This scale is best suited for evaluating people with MMSE scores below 15/30, or equivalent. Questions are administered to a qualified caregiver informant about a set of 19 basic and instrumental ADL. Instrumental ADL are selected to be relevant to this level of severity of dementia, e.g., obtaining a beverage, turning lights on and off, turning a faucet on and off. Performance of each of these activities during the past 4 weeks, as well as the level of performance, are rated. A total score is derived by summing scores across items, and ranges from 0 (maximal impairment) to 54 (maximally independent function).~This outcome is the change from baseline to week 12." (NCT03710642)
Timeframe: 12 weeks

Interventionscore on a scale (Least Squares Mean)
Treatment (Prazosin)-1.47055
Placebo Oral Capsule-4.53993

ADCS-Clinical Global Impression of Change in Agitation (ADCS-CGIC-A)

"The ADCS-CGIC-A is the primary outcome measure. It will be anchored to disruptive agitation, the target behaviors in this study. It measures whether the effects of active treatment are substantial enough to be detected by a skilled and experienced clinician on the basis of a direct examination of the participant and an interview of the participant's primary caregiver and other LTC facility staff. The baseline assessment is qualitative therefore there is no score at baseline; post-baseline scores represent a change score compared to baseline.~The ADCS-CGIC-A is a 7-point scale that is structured as the clinician's assessment of change from baseline compared to the ADCS-CGIC-A Baseline Worksheet. There is no baseline score; post-baseline scores range from 1 (improvement) to 7 (worsening). A score of 1-2 indicates clinically meaningful improvement; a score of 3-5 indicates no clinically meaningful change; a score of 6-7 indicates clinically meaningful worsening." (NCT03710642)
Timeframe: From Baseline through Week 12.

Interventionscore on a scale (Least Squares Mean)
Treatment (Prazosin)3.434
Placebo Oral Capsule3.442

Caregiver Distress on NPI/NPI-NH

"Comparison of effects on caregiver distress/occupational disruptiveness scores on the NPI/NPI-NH. Minimum score is 0 and maximum score is 60. A higher score is a worse outcome.~This outcome is the change from baseline to week 12." (NCT03710642)
Timeframe: 12 weeks

Interventionscore on a scale (Least Squares Mean)
Treatment (Prazosin)-2.4438
Placebo Oral Capsule0.9446

Neuropsychiatric Inventory (NPI)/Neuropsychiatry Inventory-Nursing Home Version (NPI-NH)

"The NPI was designed to characterize the neuropsychiatric symptoms and psychopathology of patients with AD and other dementias residing in the community about which information was obtained from family caregivers. The content of the questions and their scoring in the NPI-NH are identical to those of the NPI except for some slight rephrasing to be consistent with the LTC environment where information is gathered from professional caregivers. Assessment of the impact of behavioral disturbances on family and professional caregivers, is assessed by a caregiver distress scale in the NPI and an occupational disruptiveness scale in the NPI-NH; scoring of this component remains identical. Minimum score is 0 and highest score is 144. A higher score means a worse outcome.~This outcome is the change from baseline to week 12." (NCT03710642)
Timeframe: 12 weeks

Interventionunits on a scale (Least Squares Mean)
Treatment (Prazosin)-6.033
Placebo Oral Capsule5.506

Rescue Medication: Total mg Lorazepam Administered

Cumulative total dose of Lorazepam rescue medication administered during the trial. Information on the total mg rescue lorazepam administered will be collected as additional secondary outcome measures. If prazosin is more effective than placebo, it is predicted that participants randomized to prazosin will be prescribed lower cumulative mg of rescue lorazepam for management of persistent or worsening disruptive agitation. (NCT03710642)
Timeframe: 12 weeks

Interventionmg (Mean)
Treatment (Prazosin)0.25
Placebo Oral Capsule0.14

Responder Analysis on CGIC-A

Comparison of proportions of responders versus non responders on the ADCS-CGIC-A. Responders are defined as those with moderate or marked improvement in agitation symptoms compared to baseline assessment. (NCT03710642)
Timeframe: 12 weeks

InterventionParticipants (Count of Participants)
Treatment (Prazosin)7
Placebo Oral Capsule1

Study Discontinuations

Cox proportional hazard modelling comparing the median time to drop out between treatment groups. (NCT03710642)
Timeframe: 12 weeks

Interventiondays (Median)
Treatment (Prazosin)65.63
Placebo Oral Capsule54.62

Reviews

1 review available for dihydroxyphenylalanine and Acute Confusional Senile Dementia

ArticleYear
Oxidative stress in Parkinson's disease and other neurodegenerative disorders.
    Pathologie-biologie, 1996, Volume: 44, Issue:1

    Topics: Alzheimer Disease; Basal Ganglia Diseases; Cell Death; Dihydroxyphenylalanine; Dopamine Agents; Glut

1996

Trials

1 trial available for dihydroxyphenylalanine and Acute Confusional Senile Dementia

ArticleYear
Striatal Blood-Brain Barrier Opening in Parkinson's Disease Dementia: A Pilot Exploratory Study.
    Movement disorders : official journal of the Movement Disorder Society, 2022, Volume: 37, Issue:10

    Topics: Alzheimer Disease; Amyloid beta-Peptides; Blood-Brain Barrier; Corpus Striatum; Dementia; Dihydroxyp

2022

Other Studies

12 other studies available for dihydroxyphenylalanine and Acute Confusional Senile Dementia

ArticleYear
Dopamine neuronal loss contributes to memory and reward dysfunction in a model of Alzheimer's disease.
    Nature communications, 2017, 04-03, Volume: 8

    Topics: Alzheimer Disease; Animals; Apoptosis; Cell Death; Dendritic Spines; Dihydroxyphenylalanine; Disease

2017
Structure-activity relationship of clovamide and its related compounds for the inhibition of amyloid β aggregation.
    Bioorganic & medicinal chemistry, 2018, 07-23, Volume: 26, Issue:12

    Topics: Alzheimer Disease; Amyloid beta-Peptides; Cacao; Catechols; Cinnamates; Dihydroxyphenylalanine; Huma

2018
Covariance statistics and network analysis of brain PET imaging studies.
    Scientific reports, 2019, 02-21, Volume: 9, Issue:1

    Topics: Aged; Aged, 80 and over; Alzheimer Disease; Brain; Case-Control Studies; Cross-Sectional Studies; Di

2019
Dopamine and L-dopa disaggregate amyloid fibrils: implications for Parkinson's and Alzheimer's disease.
    FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2004, Volume: 18, Issue:9

    Topics: alpha-Synuclein; Alzheimer Disease; Amyloid; Amyloid beta-Peptides; Animals; Brain; Chromatography,

2004
Monoamine metabolites in human cerebrospinal fluid. HPLC/ED method.
    Acta neurologica Scandinavica, 1984, Volume: 69, Issue:4

    Topics: 3,4-Dihydroxyphenylacetic Acid; Alzheimer Disease; Chromatography, High Pressure Liquid; Depression;

1984
Assessment of dopamine metabolism in brain of patients with dementia by means of 18F-fluorodopa and PET.
    Annals of nuclear medicine, 1994, Volume: 8, Issue:4

    Topics: Aged; Alzheimer Disease; Analysis of Variance; Brain; Corpus Striatum; Dementia; Dementia, Vascular;

1994
Striatal dopamine metabolism correlated with frontotemporal glucose utilization in Alzheimer's disease: a double-tracer PET study.
    Neurology, 1997, Volume: 49, Issue:4

    Topics: Aged; Alzheimer Disease; Brain; Corpus Striatum; Dihydroxyphenylalanine; Dopamine; Female; Fluorodeo

1997
Patterns of cerebrospinal fluid catechols support increased central noradrenergic responsiveness in aging and Alzheimer's disease.
    Biological psychiatry, 1999, Sep-15, Volume: 46, Issue:6

    Topics: Adrenergic alpha-Agonists; Adrenergic alpha-Antagonists; Aged; Aging; Alzheimer Disease; Antimetabol

1999
Positron emission tomography in degenerative disorders of the dopaminergic system.
    Journal of neural transmission. Parkinson's disease and dementia section, 1992, Volume: 4, Issue:2

    Topics: Adult; Aged; Alzheimer Disease; Basal Ganglia; Brain; Brain Stem; Deoxyglucose; Dihydroxyphenylalani

1992
Neuropathological features of Alzheimer's disease in non-demented parkinsonian patients.
    Journal of neurology, neurosurgery, and psychiatry, 1992, Volume: 55, Issue:6

    Topics: Alzheimer Disease; Dihydroxyphenylalanine; Female; Humans; Male; Movement Disorders; Parkinson Disea

1992
Analysis of monoamines in the cerebrospinal fluid of Chinese patients with Alzheimer's disease.
    Annals of the New York Academy of Sciences, 1991, Volume: 640

    Topics: 3,4-Dihydroxyphenylacetic Acid; Alzheimer Disease; China; Chromatography, High Pressure Liquid; Dihy

1991
Simultaneous liquid-chromatographic determination of 3,4-dihydroxyphenylglycol, catecholamines, and 3,4-dihydroxyphenylalanine in plasma, and their responses to inhibition of monoamine oxidase.
    Clinical chemistry, 1986, Volume: 32, Issue:11

    Topics: Alzheimer Disease; Animals; Catecholamines; Chromatography, Liquid; Depression; Dihydroxyphenylalani

1986