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Related Concept Videos

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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Alzheimer's Disease: Treatment01:22

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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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Dementia01:30

Dementia

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Dementia is a collective term for cognitive disorders primarily affecting memory, thinking, and reasoning. It is not a specific disease but a syndrome, with Alzheimer's disease being the most common cause, accounting for approximately 60-80% of cases. Other types include vascular dementia, Lewy body dementia, and frontotemporal dementia. Dementia affects millions worldwide, particularly older adults, though it is not a normal part of aging.
The progression of dementia is generally gradual....
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Parkinson's Disease: Overview01:15

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Neurodegenerative disorders are progressive diseases that cause irreversible damage and loss to neurons in specific brain areas. Examples of these disorders include Parkinson's disease, Alzheimer's disease, Multiple Sclerosis (MS), and Amyotrophic Lateral Sclerosis (ALS). These disorders share characteristics such as proteinopathies, selective neuronal vulnerability, and a complex interplay between genetic and environmental factors. The primary therapeutic goal for these conditions is...
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Amyloid Fibrils03:03

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Amyloid fibrils are aggregates of misfolded proteins.  Under most circumstances, misfolded proteins are either refolded by chaperone proteins or degraded by the proteasome. However, in the case of a mutation or a disease, these proteins can accumulate to form large clusters and often further assemble to form elongated fibers, called fibrils. 
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Role of Neurotransmitters in Memory01:23

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Neurotransmitters are integral to the brain's communication system, enabling neurons to transmit signals across synapses. This chemical exchange underpins various cognitive functions, including memory processes. The role of neurotransmitters in memory is multifaceted, influencing the encoding, consolidation, and retrieval of memories through their action on different neural circuits.
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Hybrid PET/MRI Imaging of Alzheimer's Disease Based on 18F-AV-1451
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Hybrid PET/MRI Imaging of Alzheimer's Disease Based on 18F-AV-1451

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Alzheimer disease.

David S Knopman1, Helene Amieva2, Ronald C Petersen3

  • 1Department of Neurology, Mayo Clinic, Rochester, MN, USA. knopman@mayo.edu.

Nature Reviews. Disease Primers
|May 14, 2021
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Summary
This summary is machine-generated.

Alzheimer disease (AD) is a neurodegenerative disorder characterized by amyloid plaques and tau tangles. Current research explores the complex interplay of synaptic and clearance pathway dysfunction in AD, with ongoing challenges in developing effective therapies.

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Area of Science:

  • Neuroscience
  • Neuropathology
  • Genetics

Background:

  • Alzheimer disease (AD) is biologically defined by β-amyloid plaques and tau tangles.
  • It presents as a genetic and sporadic neurodegenerative disease causing cognitive impairment.
  • Clinical impact is influenced by co-occurring neurodegenerative and cerebrovascular conditions.

Purpose of the Study:

  • To conceptualize Alzheimer disease (AD) biology.
  • To explore the interplay between synaptic homeostasis and endosomal/lysosomal clearance pathways.
  • To identify therapeutic targets within this complex biological framework.

Main Methods:

  • Review and synthesis of current understanding of AD pathology.
  • Analysis of the roles of Aβ and tau precursors and their modified products.
  • Examination of endosomal/lysosomal clearance pathway dysfunction.

Main Results:

  • AD involves a complex interplay of lost synaptic homeostasis.
  • Dysfunction in interrelated endosomal/lysosomal clearance pathways is critical.
  • Aβ and tau species play significant roles in disease pathogenesis.

Conclusions:

  • Therapeutic strategies are challenged by the complexity of AD biology.
  • Targeting synaptic and clearance pathways offers potential avenues.
  • Substantially altering the clinical course of AD remains an ongoing challenge.