Mechanism of Alzheimer's Disease
Summary
TLDRThe video script delves into the complexities of Alzheimer's disease (AD), highlighting its early indicators such as subjective memory complaints and a decline in daily performance, particularly in individuals over 65. It explains that AD is a progressive condition with pathological changes occurring decades before clinical symptoms. The script outlines the two main pathological markers of AD: amyloid-beta plaques outside neurons and tau protein neurofibrillary tangles within them. It discusses the role of amyloid-beta in the disease's progression, its production, and accumulation, and how it can lead to inflammation and neuronal damage. The video also touches on the importance of tau protein, which becomes abnormally phosphorylated in AD, leading to the formation of neurofibrillary tangles. The script emphasizes the interplay between amyloid-beta and tau, suggesting a potential amplification of their toxic effects. It concludes by noting that while AD is often diagnosed in its later stages, ongoing research is enhancing our understanding and aiding in the development of improved diagnostic tools and potential treatments for this debilitating disease.
Takeaways
- 🧠 Alzheimer's disease (AD) is a progressive condition that can begin with subtle symptoms like memory complaints and a decline in daily activities, particularly in those over 65 years old.
- 📈 AD accounts for up to 80% of all dementia cases and is characterized by pathological changes that can occur decades before clinical symptoms appear.
- 🧪 Current diagnostic methods for AD include the assessment of biomarkers and cognitive performance tests to evaluate functional impairment and behavioral symptoms.
- 📍 The two main pathological hallmarks of AD are amyloid-beta (Aβ) plaques outside neurons and neurofibrillary tangles composed of tau protein inside neurons.
- ⏳ Abnormal accumulation of Aβ in the brain may start many years before symptoms of AD are evident and can be detected by PET scans and through low levels in cerebrospinal fluid (CSF).
- 🔍 Aβ is produced normally in the brain but can be overproduced or inadequately cleared, leading to accumulation and plaque formation, which begins in the neocortex and spreads to other brain areas.
- 🔥 The accumulation of amyloid plaques can trigger a chronic inflammatory response and disrupt the energy supply of neurons, causing further damage.
- 🧬 Tau pathology typically emerges about 15 years before the onset of AD symptoms and involves abnormal phosphorylation and aggregation into neurofibrillary tangles.
- 🔗 There is evidence that the toxic effects of tau and Aβ may amplify each other in the brain of individuals with AD.
- 🧵 As AD progresses, it leads to synaptic dysfunction, neuronal loss, and cortical atrophy, causing more advanced symptoms and spreading to brain regions controlling basic functions.
- ⏳ AD is often diagnosed in the mild dementia stage, with an average survival of 4 to 8 years post-diagnosis, although this can vary.
- 🚀 Ongoing research is enhancing our understanding of AD, with emerging risk factors, improved screening tools, and novel techniques for detecting and measuring AD biomarkers.
Q & A
What are the early signs that may indicate the onset of Alzheimer's disease (AD)?
-Early signs of AD may include subjective memory complaints and a decline in the performance of daily activities, particularly in patients aged 65 or older.
What is the nature of Alzheimer's disease (AD) in terms of its progression?
-AD is a progressive disease that begins with pathological changes occurring decades before clinical symptoms, leading to mild cognitive impairment, functional symptoms, and eventually dementia.
How is AD diagnosed in its early stages?
-AD can be diagnosed in its early symptomatic stages by assessing biomarkers and using tests to evaluate cognitive performance, functional impairment, and behavioral symptoms.
What are the two pathological hallmarks of AD and where do they typically appear in the brain?
-The two pathological hallmarks of AD are amyloid-beta (Aβ) plaques, which occur outside of neurons, and neurofibrillary tangles composed of tau protein, which develop within neurons. Aβ plaques first appear in the neocortex and progress to the hippocampus and related structures, while tau pathology begins to appear approximately 15 years before the onset of clinical AD symptoms.
How is amyloid-beta (Aβ) formed and what are the factors that can lead to its accumulation in the brain?
-Amyloid-beta is produced when amyloid precursor protein (APP) is cleaved by beta-secretase and then by gamma-secretase. Overproduction of Aβ and inadequate clearance mechanisms can cause Aβ peptides to accumulate in the brain and form plaques.
What is the role of positron emission tomography (PET) in detecting AD?
-Positron emission tomography (PET) can detect evidence of amyloid-beta deposition and plaques, which are indicative of AD pathology.
How does the accumulation of amyloid-beta plaques affect neurons?
-The accumulation of amyloid-beta plaques can activate cells of the neuronal immune system, potentially causing a chronic inflammatory reaction with toxic effects on neurons. Aβ may also disrupt the energy supply of neurons and induce oxidative stress, causing further cellular injury.
What is the relationship between tau protein and microtubules in neurons?
-Tau protein is normally associated with microtubules, which maintain structural and transport systems within neurons. In AD, the presence of amyloid-beta may promote the abnormal phosphorylation of tau, leading to its detachment from microtubules and the formation of neurofibrillary tangles.
How do the toxic effects of tau and amyloid-beta interact in the brain of a person with AD?
-There is growing evidence that the toxic effects of tau and amyloid-beta may amplify each other in the brains of people with AD, leading to further neuronal dysfunction and loss.
What happens as the pathology of AD progresses and spreads to different regions of the brain?
-As AD progresses, the pathology extends to different parts of the brain, leading to more advanced symptoms. Eventually, it spreads to regions controlling basic functions such as heart rate, ultimately leading to death.
What is the average survival time after the diagnosis of AD and what factors can influence this?
-The average survival time after the diagnosis of AD is four to eight years, but it can be longer depending on other factors such as the individual's overall health and the progression of the disease.
How is ongoing research expected to impact the understanding and treatment of AD?
-Ongoing and future research is expected to enhance our understanding of the underlying disease processes and the sequence in which they occur. This includes the identification of emerging risk factors, improved screening tools for more accurate symptom evaluation, and novel techniques for the detection and measurement of AD biomarkers, which may aid in developing better treatments for this complex disease.
Outlines
🧠 Understanding Alzheimer's Disease Pathogenesis
The first paragraph of the script delves into the early signs of Alzheimer's disease (AD), such as memory complaints and a decline in daily activities, particularly in the elderly. It explains that AD is a progressive disease with pathological changes that can occur years before symptoms are evident. The paragraph outlines the diagnostic methods available today, including biomarker assessment and cognitive performance tests. The script also discusses the pathological hallmarks of AD: amyloid-beta plaques outside neurons and tau protein neurofibrillary tangles inside neurons. It details the production and accumulation of amyloid-beta, its detection through imaging techniques, and its role in triggering inflammation and oxidative stress. The paragraph further explains how tau pathology emerges and its interaction with amyloid-beta, leading to synaptic dysfunction and neuronal loss. The progression of the disease and its impact on brain regions controlling basic functions is also described, concluding with the typical diagnosis stage and survival rates after diagnosis.
🔬 Emerging Diagnostics and Research in Alzheimer's Disease
The second paragraph focuses on the silent, early processes of AD that only become symptomatic much later. It discusses how the diagnosis of AD is being improved by new risk factor evidence, more accurate symptom-evaluating screening tools, and novel techniques for detecting and measuring AD biomarkers. The paragraph emphasizes the hope that ongoing and future research will further clarify the causes of AD and contribute to better treatment options for this complex disease. The script ends on a hopeful note, suggesting that a deeper understanding of the disease processes and their sequence is within reach.
Mindmap
Keywords
💡Alzheimer's Disease (AD)
💡Mild Cognitive Impairment (MCI)
💡Biomarkers
💡Amyloid Beta
💡Neurofibrillary Tangles
💡Cerebrospinal Fluid (CSF)
💡Positron Emission Tomography (PET)
💡Neuronal Loss
💡Cortical Atrophy
💡Dementia
💡Neurodegenerative Diseases
Highlights
Alzheimer's disease (AD) is a progressive disease that begins with pathological changes occurring decades before clinical symptoms.
AD accounts for up to 80% of all dementia diagnoses.
Diagnosis of AD in its early symptomatic stages is possible by assessing biomarkers and evaluating cognitive performance, functional impairment, and behavioral symptoms.
The two pathological hallmarks of AD are amyloid-beta plaques outside neurons and neurofibrillary tangles composed of tau protein inside neurons.
Abnormal accumulation of amyloid-beta in the brain may begin decades before symptoms appear.
Amyloid-beta is produced during normal brain metabolism but may be overproduced in certain individuals.
Healthy individuals clear amyloid-beta from the brain through systemic circulation and microglia uptake.
Overproduction and inadequate clearance of amyloid-beta can cause plaque accumulation and self-aggregation in the brain.
Amyloid-beta plaque deposition first occurs in the neocortex and progresses to the hippocampus and related structures.
Positron emission tomography can detect amyloid-beta deposition and plaques.
Low levels of amyloid-beta in cerebrospinal fluid can indicate pathology.
Accumulation of amyloid-beta activates neuronal immune cells, potentially causing chronic inflammation and toxic effects on neurons.
Tau protein pathology begins to appear around 15 years before clinical AD symptoms.
Abnormal phosphorylation of tau and its detachment from microtubules leads to the formation of neurofibrillary tangles.
Tau pathology is specific to AD, while amyloid-beta may also be present in other neurodegenerative diseases.
Growing evidence suggests that the toxic effects of tau and amyloid-beta may amplify each other in AD.
AD pathology causes synaptic dysfunction, neuronal loss, and cortical atrophy, leading to more advanced symptoms as the disease progresses.
AD is often diagnosed in the mild AD dementia stage, with an average survival of 4-8 years after diagnosis.
Ongoing research is enhancing our understanding of the underlying disease processes and sequence in AD.
Emerging risk factor evidence, improved screening tools, and novel techniques for detecting/ measuring AD biomarkers are aiding in the diagnosis of the earliest stages of AD.
It is hoped that future research will help unravel the causes of AD and lead to better treatment options for this complex disease.
Transcripts
the mysteries and paths of alzheimer's
disease
subjective memory complaints and a
decline of performance of daily
activities may indicate early stages of
alzheimer's disease or a.d
particularly in patients age 65 or older
ad is a progressive disease beginning
with pathological changes that occur
decades before clinical symptoms leading
eventually to the development of mild
cognitive impairment
functional symptoms and then dementia
ad accounts for as many as 80 percent of
all dementia diagnoses
today we are able to diagnose ad in its
early symptomatic stages by assessing
biomarkers and by using tests to
evaluate cognitive performance
functional impairment and behavioral
symptoms
to better understand the disease we must
look back in time to the pathological
origins of a.d within the brain
the two pathological hallmarks of ad
appear at distinct locations within the
brain plaques made up of a beta occur
outside of neurons
while neurofibrillary tangles composed
of tau protein develop within neurons
abnormal accumulation of a beta within
the brain may begin decades before
symptoms appear
amyloid beta is produced when amyloid
precursor protein or app
is cleaved by beta secretase base 1
and then by gamma secretase
a beta is formed in the course of normal
brain metabolism
however it may be over produced in
certain individuals
in healthy people a beta is cleared from
the brain through systemic circulation
and local processes such as uptake by
microglia
both the overproduction of a beta and
inadequate clearance mechanisms can
cause a beta peptides to accumulate in
the brain and self-aggregate into
plaques plaque deposition is first seen
in the brain's neocortex the center of
higher mental functions it progresses to
the more primitive cortex including the
hippocampus and related structures
involved in learning and memory
finally it spreads to subcortical areas
that regulate attention emotion and
various other activities positron
emission tomography can detect evidence
of a beta deposition and plaques low
levels of a beta and cerebrospinal fluid
or csf can also indicate pathology
over time the accumulation of amyloid
plaques activates cells of the neuronal
immune system potentially causing a
chronic inflammatory reaction that has
toxic effects on neurons
a beta may also disrupt the energy
supply of neurons and induce oxidative
stress causing further cellular injury
tau protein pathology begins to appear
approximately 15 years before the onset
of clinical ad symptoms
tau is normally associated with
microtubules which maintains structural
and transport systems within neurons
in people with ad the presence of a beta
may promote the abnormal phosphorylation
of tau followed by its detachment of
microtubules
tau subsequently associates into
insoluble structures called paired
helical filaments which further
aggregate to form neurofibrillary
tangles higher abnormal levels of towel
can be detected in the cerebrospinal
fluid
[Music]
while neurofibrillary tangles may appear
in the brains of people with other
neurodegenerative diseases there is
growing evidence that the toxic effects
of tau and a beta may amplify each other
in people with ad
eventually the underlying pathology of
ad causes synaptic dysfunction and
neuronal loss
this results in cortical thinning or
atrophy leading to more advanced
symptoms
as the disease progresses it extends to
different parts of the brain with
corresponding biomarker evidence of
pathology
as more regions are affected more
symptoms appear
over time pathology spreads to regions
of the brain that control basic
functions such as heart rate
leading ultimately to death a.d is often
diagnosed in the mild a d dementia stage
and average survival is four to eight
years after the diagnosis of ad but can
be longer depending on other factors
with ongoing advances in ad research we
continue to enhance our understanding of
underlying disease processes and the
sequence in which they occur we now know
that a.d begins with clinically silent
processes which lead to the appearance
of symptoms decades later diagnosis of
the earliest stages of ad is being aided
by emerging risk factor evidence
improved screening tools that evaluate
symptoms with greater accuracy and novel
techniques for the detection and
measurement of ad biomarkers
it is hoped that ongoing and future
research continues to help unravel the
causes of ad
and hopefully aids in better treatment
of this complex disease
[Music]
you
Parcourir plus de vidéos associées
![](https://i.ytimg.com/vi/8wJRWRpUrCc/hq720.jpg?sqp=-oaymwEmCIAKENAF8quKqQMa8AEB-AHUBoAC4AOKAgwIABABGHIgPCg4MA8=&rs=AOn4CLDOI0f5bZqBLO2rlwzn14HWURycog)
Dyslexia and the Brain 2
![](https://i.ytimg.com/vi/aU67LeF07tY/hq720.jpg)
COMO FUNCIONA O LEILÃO DO GOOGLE ADS? QUAIS OS PILARES E COMO VENCER C/ POUCA VERBA? [AVANÇADO]
![](https://i.ytimg.com/vi/LI353q_aQPs/hq720.jpg)
The Science Behind The Most Underrated Supplement | L-Carnitine
![](https://i.ytimg.com/vi/PB_Ln5HXkwQ/hq720.jpg)
The REAL Cause of Tremors (Essential)
![](https://i.ytimg.com/vi/csxdPCdmMyY/hq720.jpg)
ОРГАНИЗМ САМ НАЧНЕТ ВОССТАНАВЛИВАТЬСЯ! Узнайте, что нужно ИМЕННО ВАМ!
![](https://i.ytimg.com/vi/zoxszhv9D1k/hq720.jpg)
The True Origins of Lyme Disease
5.0 / 5 (0 votes)