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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

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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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

Parkinson's Disease: Overview

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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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Role of Neurotransmitters in Memory01:23

Role of Neurotransmitters in Memory

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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.
 Glutamate and Synaptic Plasticity
Glutamate, the brain's main excitatory neurotransmitter, is...
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Amyloid Fibrils03:03

Amyloid Fibrils

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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. 
Amyloid deposits were observed as early as 1639 in the liver and the spleen.   In 1854, Rudolph Virchow performed iodine staining,...
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Alzheimer's disease basics: we all should know.

Sayantan Das1

  • 1School of Computer and Systems Sciences, Jawaharlal Nehru University, New Delhi, India.

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Alzheimer's disease involves protein buildup and neuroinflammation. Monoclonal antibodies show promise in slowing cognitive decline but require careful patient selection and safety monitoring for effective treatment.

Keywords:
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Area of Science:

  • Neuroscience
  • Immunology
  • Genetics

Background:

  • Alzheimer's disease (AD) is a leading cause of dementia, impacting millions globally with progressive cognitive decline.
  • Pathological hallmarks include amyloid-beta (Aβ) plaques, neurofibrillary tangles (NFTs) of tau protein, and chronic neuroinflammation.

Purpose of the Study:

  • To review the molecular, genetic, and immunological factors contributing to Alzheimer's disease.
  • To focus on pathogenic proteins, glial cell roles, and current monoclonal antibody (mAb) therapies.

Main Methods:

  • Literature review of key players: Aβ, tau, microglia, and astrocytes.
  • Analysis of genetic mutations (APP, PSEN1, PSEN2, APOE, BACE1, MAPT) and their impact.
  • Review of clinical trial data for anti-Aβ mAbs (aducanumab, lecanemab, donanemab).

Main Results:

  • Neuroinflammation exacerbates AD pathology, leading to synaptic loss and neuronal death.
  • Monoclonal antibodies demonstrate potential in reducing Aβ burden and slowing cognitive decline (e.g., donanemab, lecanemab).
  • Adverse events like ARIA are significant, especially in APOE-4 carriers; aducanumab was discontinued.

Conclusions:

  • AD is multifactorial, involving protein aggregation, immune response, and genetic predisposition.
  • mAb therapies offer disease modification potential but require precise patient stratification and safety monitoring.
  • Future strategies necessitate personalized, combinatorial approaches integrating biomarkers and advanced technologies for AD management.