Prodromal Alzheimer's
Prodromal Alzheimer's - Related Videos
11:01
Examining the Characteristics of Episodic Memory using Event-related Potentials in Patients with Alzheimer's Disease
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2011
The methodology for collecting high-density event-related potential data while patients with Alzheimer's disease perform a recognition memory task is reviewed. This protocol will include subject preparation, quality assurance, data acquisition, and data analysis.
01:22
Alzheimer's Disease: Treatment
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2024
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...
01:29
Alzheimer Disease l: Introduction
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2026
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...
06:02
Detection of Neuritic Plaques in Alzheimer's Disease Mouse Model
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Cited by 66 •
2011
One of the pathological characteristics of AD is the formation of Amyloid β protein positive neuritic plaques. In this protocol we describe two methods to detect neuritic plaques in transgenic AD model mice: immunohistochemical detection using the ABC and DAB method and fluorescent detection using thioflavin S staining method.
01:17
Immunofluorescent Staining of Heparan Sulfate in Amyloid Plaques of Alzheimer's Disease
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2025
To visualize heparan sulfate, begin with a diseased human hippocampal tissue section containing amyloid plaques.
FAQs
Amyloid-beta accumulation and abnormal tau phosphorylation can injure synapses, the communication points between neurons, and disrupt neural networks. These changes help explain why memory problems and other measurable cognitive difficulties may emerge while daily functioning remains comparatively preserved. Studying this relationship connects molecular pathology with the cognitive findings used to identify Alzheimer’s-related impairment.
Cognitive testing measures the observable effects of impairment, including changes in memory and other abilities. Brain imaging and cerebrospinal fluid biomarkers provide biological evidence associated with Alzheimer’s disease. Considering these sources together helps researchers distinguish Alzheimer’s-related cognitive decline from other causes more effectively than relying on cognitive performance or biological measures alone.
Researchers can follow changes across several levels: performance on memory and other cognitive tasks, evidence from brain imaging, and biomarkers measured in cerebrospinal fluid. Together, these measures reflect alterations in synapses and neural networks associated with amyloid-beta accumulation and abnormal tau phosphorylation. Repeated assessment supports monitoring as impairment changes over time.
Evaluation combines cognitive testing with biomarker assessment rather than treating a single result as sufficient. Researchers examine memory and other cognitive abilities, then consider relevant findings from brain imaging and cerebrospinal fluid. This integrated approach helps characterize Alzheimer’s-related impairment, compare it with other causes of decline, and establish measures for follow-up.
This stage is valuable for clinical trials because participants show measurable cognitive changes before extensive neuronal loss has occurred. Studying interventions earlier may allow researchers to evaluate whether a treatment influences disease-related impairment while there is still an opportunity to observe changes in cognition, biomarkers, or neural systems during follow-up.
It provides a neuroscience framework for linking molecular changes to behavior. Amyloid-beta and abnormal tau phosphorylation are associated with damage to synapses and neural networks, while cognitive testing captures resulting changes in memory and other abilities. This connection allows researchers to study how alterations at cellular and network levels appear as measurable cognitive impairment.