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Related Concept Videos

Alzheimer Disease ll: Pathophysiology01:23

Alzheimer Disease ll: Pathophysiology

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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...
32
Alzheimer Disease l: Introduction01:29

Alzheimer Disease l: Introduction

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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...
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Alzheimer's Disease: Overview01:26

Alzheimer's Disease: Overview

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Alzheimer's Disease (AD) is a continually advancing neurodegenerative disorder, distinguished by escalating memory loss, cognitive dysfunction, and dementia. The disease unfolds in three stages: preclinical, mild cognitive impairment (MCI), and dementia. Its onset is insidious, and the progression gradual, with the cause not well explained by other disorders.
The clinical diagnosis of AD hinges on the presence of memory and other cognitive impairments. Biomarkers, such as changes in Aβ...
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Dementia l: Introduction01:22

Dementia l: Introduction

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Dementia is an acquired, progressive syndrome characterized by a decline in multiple cognitive domains severe enough to impair daily functioning and reduce independence. Although memory loss is a central feature, the diagnosis requires additional deficits involving language, executive function, visuospatial skills, judgment, calculation, or abstract reasoning. These cognitive impairments reflect underlying neurodegenerative or vascular processes that gradually disrupt neuronal networks...
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Alzheimer's Disease: Treatment01:22

Alzheimer's Disease: Treatment

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Alzheimer's Disease (AD), a neurodegenerative disorder, is pathologically identified by amyloid plaques and neurofibrillary tangles composed of tau protein. AD pharmacotherapy aims to manage cognitive symptoms, delay disease progression, and treat behavioral symptoms. The treatment is primarily symptomatic and palliative, with no definitive disease-modifying therapy available. Cholinesterase inhibitors, including donepezil (Aricept), rivastigmine (Exelon), and galantamine (Razadyne), are...
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Parkinson Disease ll: Pathophysiology01:24

Parkinson Disease ll: Pathophysiology

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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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Related Experiment Video

Updated: Apr 28, 2026

Motor and Hippocampal Dependent Spatial Learning and Reference Memory Assessment in a Transgenic Rat Model of Alzheimer's Disease with Stroke
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PLD3 in Alzheimer's disease.

Jun Wang1, Jin-Tai Yu, Lan Tan

  • 1Department of Neurology, Qingdao Municipal Hospital, School of Medicine, Qingdao University, Qingdao, China.

Molecular Neurobiology
|June 18, 2014
PubMed
Summary

Rare variants in the phospholipase D3 (PLD3) gene are linked to increased Alzheimer's disease risk. Lower PLD3 levels in Alzheimer's brains suggest a role in disease progression and potential therapeutic targets.

Area of Science:

  • Neurogenetics
  • Molecular Biology
  • Biochemistry

Background:

  • Rare coding variants in the phospholipase D3 (PLD3) gene are associated with increased risk for late-onset Alzheimer's disease (LOAD).
  • PLD3 is highly expressed in brain neurons, with lower levels in other tissues.
  • PLD3 expression is downregulated in Alzheimer's disease (AD) brains.

Purpose of the Study:

  • To summarize the biochemical properties of PLD3.
  • To review genetic and expression findings of PLD3 related to AD.
  • To speculate on the role of PLD3 in AD pathogenesis and progression.

Main Methods:

  • Whole exome sequencing (WES) in LOAD families.
  • Follow-up analyses of candidate variants in independent LOAD case-control data series.

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  • Review of existing literature on PLD3 genetics and expression in AD.

    • Main Results:

    • PLD3 variants identified as risk factors for LOAD.
    • Downregulation of PLD3 in AD brains, negatively correlated with amyloid precursor protein (APP) and amyloid-beta (Aβ) levels.
    • PLD3 may influence AD pathogenesis via APP processing.

    Conclusions:

    • PLD3 plays a role in AD pathogenesis.
    • Targeting PLD3 presents a potential therapeutic strategy for Alzheimer's disease.
    • Further research into PLD3's function in AD is warranted.