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Related Concept Videos

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...
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's Disease: Overview01:26

Alzheimer's Disease: Overview

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 and tau...
Alzheimer's Disease: Treatment01:22

Alzheimer's Disease: Treatment

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...
Nonsense-mediated mRNA Decay02:27

Nonsense-mediated mRNA Decay

The Upf proteins that carry out nonsense-mediated decay (NMD) are found in all eukaryotic organisms, including humans. Each protein has an individual role, but they need to work in collaboration. Upf1 is an ATP-dependent RNA helicase that unwinds the RNA helix. Because Upf1 can unwind any RNA, Upf2 and Upf3 are required to help Upf1 discriminate between nonsense and normal mRNAs.
Usually, Upf3 binds to an Exon Junction Complex (EJC) at mRNA splice sites. If a ribosome fully translates the mRNA,...
lncRNA - Long Non-coding RNAs02:39

lncRNA - Long Non-coding RNAs

In humans, more than 80% of the genome gets transcribed. However, only around 2% of the genome codes for proteins. The remaining part produces non-coding RNAs which includes ribosomal RNAs, transfer RNAs, telomerase RNAs, and regulatory RNAs, among other types. A large number of regulatory non-coding RNAs have been classified into two groups depending upon their length – small non-coding RNAs, such as microRNA, which are less than 200 nucleotides in length, and long non-coding RNA (lncRNA)...

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Mapping Alzheimer's Disease Variants to Their Target Genes Using Computational Analysis of Chromatin Configuration
04:41

Mapping Alzheimer's Disease Variants to Their Target Genes Using Computational Analysis of Chromatin Configuration

Published on: January 9, 2020

Decoding the non-coding RNAs in Alzheimer's disease.

Nicole Schonrock1, Jürgen Götz

  • 1Victor Chang Cardiac Research Institute (VCCRI), Darlinghurst, NSW 2010, Australia. n.schonrock@victorchang.edu.au

Cellular and Molecular Life Sciences : CMLS
|September 8, 2012
PubMed
Summary
This summary is machine-generated.

Non-coding RNAs (ncRNAs) are key regulators of gene expression, particularly in the human brain. This review explores their role in Alzheimer's disease (AD) and potential for new diagnostics and therapies.

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Area of Science:

  • Genetics and Molecular Biology
  • Neuroscience
  • Epigenetics

Background:

  • Non-coding RNAs (ncRNAs) are crucial for gene expression regulation.
  • ncRNAs integrate DNA, epigenetic, and protein complex information to control cellular networks.
  • Humans possess a high abundance of ncRNAs, especially in the brain, impacting development and cognition.

Purpose of the Study:

  • To review the emerging role of ncRNAs in Alzheimer's disease (AD).
  • To discuss the complexity of ncRNA regulation concerning AD-related proteins like amyloid precursor protein and Tau.
  • To highlight the potential of understanding ncRNA networks for AD diagnostics and therapeutics.

Main Methods:

  • Literature review focusing on ncRNAs and their function in gene regulation.
  • Analysis of ncRNA involvement in the biological pathways of Alzheimer's disease.
  • Examination of the regulatory interactions between ncRNAs and key AD proteins (APP, Tau).

Main Results:

  • ncRNAs play a complex, integral role in gene expression and epigenetic regulation.
  • The human brain shows a high prevalence of ncRNAs, suggesting significant roles in cognitive functions.
  • ncRNAs are implicated in the regulation of amyloid precursor protein (APP) and Tau, central to AD pathogenesis.

Conclusions:

  • Understanding the intricate ncRNA regulatory network is vital for deciphering AD mechanisms.
  • ncRNAs offer promising avenues for developing novel diagnostic and therapeutic strategies for Alzheimer's disease.
  • Further research into ncRNA function can enhance our comprehension of brain development and cognitive disorders.