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Alzheimer Disease ll: Pathophysiology01:23

Alzheimer Disease ll: Pathophysiology

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 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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BACE1 mRNA expression in Alzheimer's disease postmortem brain tissue.

David T R Coulson1, Nancy Beyer, Joe G Quinn

  • 1Queen's University Belfast, School of Medicine, Dentistry and Biomedical Sciences, Northern Ireland.

Journal of Alzheimer'S Disease : JAD
|October 9, 2010
PubMed
Summary
This summary is machine-generated.

This study investigated beta-site amyloid precursor protein cleaving enzyme 1 (BACE1) mRNA levels in Alzheimer's disease (AD) and Parkinson's disease (PD) brains. Elevated BACE1 mRNA was found in specific brain regions in AD, potentially linked to neuronal changes.

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Area of Science:

  • Neuroscience
  • Molecular Biology
  • Genetics

Background:

  • Beta-site amyloid precursor protein cleaving enzyme 1 (BACE1) is crucial for amyloid-beta (Aβ) peptide production, a key factor in Alzheimer's disease (AD) pathology.
  • Previous studies indicate elevated BACE1 protein levels and activity in AD brains, but the underlying transcriptional regulation remains unclear.
  • Understanding BACE1 mRNA expression patterns in neurodegenerative diseases is vital for elucidating AD pathogenesis.

Purpose of the Study:

  • To investigate whether elevated BACE1 protein levels in Alzheimer's disease (AD) brains are associated with increased BACE1 mRNA expression.
  • To compare BACE1 mRNA levels across different brain regions in control subjects, AD patients, and individuals with other neurodegenerative diseases like Parkinson's disease (PD) and dementia with Lewy bodies (DLB).
  • To correlate BACE1 mRNA expression with glial and neuronal marker changes in AD progression.

Main Methods:

  • RNA was extracted from five brain regions of control, AD, and PD/DLB groups.
  • BACE1 mRNA levels were quantified using quantitative real-time PCR (qPCR) and analyzed with qbasePLUS software.
  • Glial fibrillary acidic protein (GFAP) and neuron-specific enolase (NSE) mRNA levels were measured to assess glial and neuronal activity.

Main Results:

  • BACE1 mRNA levels were significantly elevated in the medial temporal and superior parietal gyri of AD patients compared to PD/DLB and control groups.
  • Superior frontal gyrus BACE1 mRNA levels were significantly increased in the PD/DLB group compared to AD and control groups.
  • In AD, increased BACE1 mRNA correlated with reduced NSE and increased GFAP mRNA, suggesting a link to neuronal loss and glial activation.

Conclusions:

  • Elevated BACE1 mRNA expression in specific brain regions of AD patients supports its role in AD pathogenesis.
  • Increased BACE1 mRNA in remaining neuronal cells may contribute to elevated BACE1 protein levels and activity observed in AD-affected brain areas.
  • Differential BACE1 mRNA expression patterns were observed between AD and PD/DLB groups, highlighting disease-specific molecular changes.