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Related Concept Videos

Alzheimer Disease l: Introduction01:29

Alzheimer Disease l: Introduction

Alzheimer disease is a chronic, progressive, and irreversible neurodegenerative disorder and the most common cause of dementia in older adults. It leads to gradual neuronal loss, causing cognitive decline, behavioral changes, and loss of functional independence.Risk Factors and EtiologyThe disease is multifactorial. Age is the strongest risk factor, with prevalence doubling every 5 years after age 65. Genetic factors include mutations in genes such as APP, PSEN1, and PSEN2, which are associated...
Alzheimer Disease ll: Pathophysiology01:23

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Alzheimer disease involves structural changes in the brain that begin long before symptoms appear. The most distinctive features are extracellular neuritic plaques and intracellular neurofibrillary tangles.Neuritic plaques form in the cerebral cortex and around blood vessels. These plaques contain a dense core of beta-amyloid (Aβ)—a toxic protein fragment that clumps outside neurons. The core is surrounded by damaged neuronal extensions, as well as reactive astrocytes and microglia. Abnormal...
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Alzheimer's Disease: Overview

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The clinical diagnosis of AD hinges on the presence of memory and other cognitive impairments. Biomarkers, such as changes in Aβ and tau...
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Parkinson disease (PD) is a progressive neurodegenerative disorder primarily affecting movement, with additional non-motor features. Its pathophysiology involves complex interactions among genetic susceptibility, environmental exposures, and cellular dysfunction, including dopaminergic neuron loss, protein aggregation, and mitochondrial impairment.Selective NeurodegenerationA key feature is the degeneration of dopaminergic neurons in the substantia nigra pars compacta, leading to reduced...
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Drugs affecting neurotransmitter synthesis can impact the adrenergic neuron and the synthesis of neurotransmitters. For example, α-methyltyrosine and carbidopa target specific enzymes involved in catecholamine synthesis. α-methyltyrosine inhibits the enzyme tyrosine hydroxylase, which converts tyrosine into dopamine. By blocking this enzyme, α-methyltyrosine reduces dopamine production and other catecholamines. Carbidopa, on the other hand, inhibits the enzyme dopa decarboxylase, which converts...

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Related Experiment Video

Updated: May 14, 2026

Assessment of Dopaminergic Homeostasis in Mice by Use of High-performance Liquid Chromatography Analysis and Synaptosomal Dopamine Uptake
11:26

Assessment of Dopaminergic Homeostasis in Mice by Use of High-performance Liquid Chromatography Analysis and Synaptosomal Dopamine Uptake

Published on: September 21, 2017

Genotype-independent decrease in plasma dopamine beta-hydroxylase activity in Alzheimer's disease.

Maja Mustapic1, Paola Presecki, Nela Pivac

  • 1Division of Molecular Medicine, Rudjer Boskovic Institute, Bijenicka 54, HR-10000 Zagreb, Croatia.

Progress in Neuro-Psychopharmacology & Biological Psychiatry
|February 19, 2013
PubMed
Summary
This summary is machine-generated.

Plasma dopamine beta-hydroxylase (DBH) activity decreases in early Alzheimer's disease (AD), suggesting a compensatory mechanism for noradrenergic neuron loss. This finding may inform early AD treatment strategies targeting noradrenaline pathways.

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Detection of Neuritic Plaques in Alzheimer's Disease Mouse Model
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Assessment of Dopaminergic Homeostasis in Mice by Use of High-performance Liquid Chromatography Analysis and Synaptosomal Dopamine Uptake
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Detection of Neuritic Plaques in Alzheimer's Disease Mouse Model
06:02

Detection of Neuritic Plaques in Alzheimer's Disease Mouse Model

Published on: July 26, 2011

Area of Science:

  • Neuroscience
  • Genetics
  • Biochemistry

Background:

  • The noradrenergic system's role in Alzheimer's disease (AD) pathogenesis is not fully understood.
  • Dopamine beta-hydroxylase (DBH) is crucial for noradrenaline (NA) synthesis, and its plasma activity (pDBH) exhibits significant genetic variability.

Purpose of the Study:

  • To investigate plasma DBH activity and the association of DBH gene polymorphisms (C-970T and C1603T) with Alzheimer's disease.
  • To explore the relationship between pDBH activity, DBH genotypes, and AD stages.

Main Methods:

  • Compared pDBH activity and DBH genotypes (C-970T, C1603T) in 207 AD patients and 90 healthy controls.
  • Utilized two-way ANOVA to analyze the effects of diagnosis and genotype on pDBH activity.
  • Assessed genotype association with AD, controlling for age, gender, and ApoE4 status.

Main Results:

  • Plasma DBH activity was significantly lower in early-stage AD patients compared to later stages and controls.
  • Both diagnosis and DBH genotypes (C-970T, C1603T) had a significant effect on pDBH activity, but no significant interaction was observed.
  • No significant association was found between AD and the studied DBH genotypes (C-970T, C1603T).

Conclusions:

  • Decreased pDBH activity in early AD may reflect a compensatory response to noradrenergic neuron loss.
  • Targeted treatments, such as selective NA reuptake inhibitors, could be beneficial in early AD stages to counteract noradrenergic deficits.