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Related Concept Videos

Alzheimer's Disease: Overview01:26

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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.
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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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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.
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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 Disease ll: Pathophysiology01:23

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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...
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Dementia l: Introduction01:22

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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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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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Alzheimer's disease.

D L Price, P J Whitehouse, R G Struble

    Annual Review of Medicine
    |January 1, 1985
    PubMed
    Summary
    This summary is machine-generated.

    Researchers are identifying brain changes in Alzheimer's disease (AD) patients, linking neurotransmitter system alterations to disease hallmarks. However, the clinical impact, cause, and effective treatments for AD remain unknown.

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    Area of Science:

    • Neuroscience
    • Neuropathology
    • Pharmacology

    Background:

    • Alzheimer's disease (AD) is characterized by progressive neurodegeneration.
    • Key neurotransmitter systems, including cholinergic, monoaminergic, and peptidergeric, show alterations in AD brains.
    • Neurobiological studies are exploring links between these neurotransmitter changes and AD's histological features.

    Purpose of the Study:

    • To summarize the current understanding of neurotransmitter system changes in Alzheimer's disease.
    • To highlight the relationship between neurotransmitter abnormalities and neuropathological hallmarks.
    • To identify knowledge gaps regarding clinical consequences, etiology, and therapeutic strategies for AD.

    Main Methods:

    • Review of neurobiological and neuropathological findings in Alzheimer's disease research.
    • Analysis of studies investigating neurotransmitter systems in AD.
    • Correlation of molecular changes with histological hallmarks like neurofibrillary tangles and senile plaques.

    Main Results:

    • Significant progress in identifying alterations in cholinergic, monoaminergic, and peptidergic systems in AD.
    • Emerging evidence links these neurotransmitter changes to neurofibrillary tangles, senile plaques, and neuronal loss.
    • The clinical significance of these neurotransmitter alterations is not yet understood.

    Conclusions:

    • While progress has been made in understanding AD neurobiology, the clinical implications of neurotransmitter changes require further investigation.
    • The definitive cause of Alzheimer's disease remains unidentified.
    • Effective therapeutic interventions for Alzheimer's disease are still lacking.