Mechanism of Alzheimer's Disease

00:06:02
https://www.youtube.com/watch?v=bQsgiBh0QCY

概要

TLDRDe ziekte van Alzheimer (AD) is een progressieve aandoening die begint met pathologische veranderingen in de hersenen, jaren voordat symptomen optreden. Het wordt gekarakteriseerd door een combinatie van plaques (a bèta) die zich buiten neuronen vormen en neurofibrillaire tangles (tau-eiwit) die binnen neuronen ontstaan. Beide leiden tot synaptische dysfunctie en uiteindelijk neuronale afsterving. Diagnose in de vroege stadia van de ziekte is mogelijk door biomarkertests en een verbeterde evaluatie van symptomen. Onderzoek naar AD vordert, wat kan leiden tot betere behandelingen.

収穫

  • 🧠 Alzheimer is een progressieve ziekte.
  • 👵 Vroege symptomen zijn geheugenklachten en functieverlies.
  • 🔬 Diagnose gebeurt door biomarkertests.
  • 🧪 Plaques en tangles zijn kenmerkend voor Alzheimer.
  • ⚠️ Aantasting van de hersenfunctie leidt tot cognitieve achteruitgang.
  • ⏳ Gemiddelde overlevingsduur na diagnose is 4-8 jaar.

タイムライン

  • 00:00:00 - 00:06:02

    Milde symptomen van geheugenverlies en een achteruitgang in dagelijkse activiteiten kunnen vroege tekenen van de ziekte van Alzheimer (AD) zijn, vooral bij mensen ouder dan 65 jaar. AD is een progressieve aandoening die begint met pathologische veranderingen jaren voordat klinische symptomen zichtbaar zijn, wat leidt tot milde cognitieve achteruitgang, functionele stoornissen en uiteindelijk dementie. AD is verantwoordelijk voor ongeveer 80 procent van de dementiediagnoses. Huidige diagnosemethoden omvatten het gebruik van biomerkers en tests voor cognitieve prestaties en gedragsymptomen.

マインドマップ

ビデオQ&A

  • Wat zijn de vroege symptomen van de ziekte van Alzheimer?

    Subjectieve geheugenklachten en verminderde prestaties in dagelijkse activiteiten.

  • Hoe wordt de ziekte van Alzheimer gediagnosticeerd?

    Door biomarkertests en beoordelingen van cognitieve prestaties, functionele beperkingen en gedragingen.

  • Wat zijn de twee belangrijkste pathologische kenmerken van Alzheimer?

    Plaques van amyloïde bèta en neurofibrillaire tangles van tau-eiwit.

  • Wat veroorzaakt de accumulatie van amyloïde bèta in de hersenen?

    Overproductie van a bèta en ontoereikende opruimmechanismen kunnen leiden tot ophoping.

  • Wat zijn de gevolgen van tau-eiwitpathologie?

    Het leidt tot synaptische dysfunctie en neuronale afsterving.

  • Hoe lang kan iemand overleven na de diagnose van Alzheimer?

    Gemiddeld vier tot acht jaar, afhankelijk van andere factoren.

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  • 00:00:00
    the mysteries and paths of alzheimer's
  • 00:00:03
    disease
  • 00:00:05
    subjective memory complaints and a
  • 00:00:07
    decline of performance of daily
  • 00:00:09
    activities may indicate early stages of
  • 00:00:12
    alzheimer's disease or a.d
  • 00:00:15
    particularly in patients age 65 or older
  • 00:00:19
    ad is a progressive disease beginning
  • 00:00:21
    with pathological changes that occur
  • 00:00:24
    decades before clinical symptoms leading
  • 00:00:26
    eventually to the development of mild
  • 00:00:28
    cognitive impairment
  • 00:00:30
    functional symptoms and then dementia
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    ad accounts for as many as 80 percent of
  • 00:00:36
    all dementia diagnoses
  • 00:00:39
    today we are able to diagnose ad in its
  • 00:00:42
    early symptomatic stages by assessing
  • 00:00:44
    biomarkers and by using tests to
  • 00:00:47
    evaluate cognitive performance
  • 00:00:50
    functional impairment and behavioral
  • 00:00:52
    symptoms
  • 00:00:53
    to better understand the disease we must
  • 00:00:56
    look back in time to the pathological
  • 00:00:58
    origins of a.d within the brain
  • 00:01:01
    the two pathological hallmarks of ad
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    appear at distinct locations within the
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    brain plaques made up of a beta occur
  • 00:01:09
    outside of neurons
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    while neurofibrillary tangles composed
  • 00:01:13
    of tau protein develop within neurons
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    abnormal accumulation of a beta within
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    the brain may begin decades before
  • 00:01:22
    symptoms appear
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    amyloid beta is produced when amyloid
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    precursor protein or app
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    is cleaved by beta secretase base 1
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    and then by gamma secretase
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    a beta is formed in the course of normal
  • 00:01:39
    brain metabolism
  • 00:01:41
    however it may be over produced in
  • 00:01:43
    certain individuals
  • 00:01:45
    in healthy people a beta is cleared from
  • 00:01:48
    the brain through systemic circulation
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    and local processes such as uptake by
  • 00:01:53
    microglia
  • 00:01:56
    both the overproduction of a beta and
  • 00:01:59
    inadequate clearance mechanisms can
  • 00:02:01
    cause a beta peptides to accumulate in
  • 00:02:04
    the brain and self-aggregate into
  • 00:02:06
    plaques plaque deposition is first seen
  • 00:02:10
    in the brain's neocortex the center of
  • 00:02:13
    higher mental functions it progresses to
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    the more primitive cortex including the
  • 00:02:17
    hippocampus and related structures
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    involved in learning and memory
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    finally it spreads to subcortical areas
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    that regulate attention emotion and
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    various other activities positron
  • 00:02:30
    emission tomography can detect evidence
  • 00:02:32
    of a beta deposition and plaques low
  • 00:02:36
    levels of a beta and cerebrospinal fluid
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    or csf can also indicate pathology
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    over time the accumulation of amyloid
  • 00:02:45
    plaques activates cells of the neuronal
  • 00:02:48
    immune system potentially causing a
  • 00:02:51
    chronic inflammatory reaction that has
  • 00:02:53
    toxic effects on neurons
  • 00:02:56
    a beta may also disrupt the energy
  • 00:02:58
    supply of neurons and induce oxidative
  • 00:03:01
    stress causing further cellular injury
  • 00:03:06
    tau protein pathology begins to appear
  • 00:03:09
    approximately 15 years before the onset
  • 00:03:11
    of clinical ad symptoms
  • 00:03:16
    tau is normally associated with
  • 00:03:18
    microtubules which maintains structural
  • 00:03:21
    and transport systems within neurons
  • 00:03:24
    in people with ad the presence of a beta
  • 00:03:27
    may promote the abnormal phosphorylation
  • 00:03:30
    of tau followed by its detachment of
  • 00:03:32
    microtubules
  • 00:03:36
    tau subsequently associates into
  • 00:03:38
    insoluble structures called paired
  • 00:03:40
    helical filaments which further
  • 00:03:42
    aggregate to form neurofibrillary
  • 00:03:45
    tangles higher abnormal levels of towel
  • 00:03:48
    can be detected in the cerebrospinal
  • 00:03:50
    fluid
  • 00:03:51
    [Music]
  • 00:03:52
    while neurofibrillary tangles may appear
  • 00:03:55
    in the brains of people with other
  • 00:03:57
    neurodegenerative diseases there is
  • 00:03:59
    growing evidence that the toxic effects
  • 00:04:01
    of tau and a beta may amplify each other
  • 00:04:04
    in people with ad
  • 00:04:07
    eventually the underlying pathology of
  • 00:04:09
    ad causes synaptic dysfunction and
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    neuronal loss
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    this results in cortical thinning or
  • 00:04:16
    atrophy leading to more advanced
  • 00:04:19
    symptoms
  • 00:04:20
    as the disease progresses it extends to
  • 00:04:22
    different parts of the brain with
  • 00:04:24
    corresponding biomarker evidence of
  • 00:04:26
    pathology
  • 00:04:28
    as more regions are affected more
  • 00:04:31
    symptoms appear
  • 00:04:33
    over time pathology spreads to regions
  • 00:04:35
    of the brain that control basic
  • 00:04:37
    functions such as heart rate
  • 00:04:39
    leading ultimately to death a.d is often
  • 00:04:42
    diagnosed in the mild a d dementia stage
  • 00:04:45
    and average survival is four to eight
  • 00:04:47
    years after the diagnosis of ad but can
  • 00:04:50
    be longer depending on other factors
  • 00:04:53
    with ongoing advances in ad research we
  • 00:04:56
    continue to enhance our understanding of
  • 00:04:59
    underlying disease processes and the
  • 00:05:01
    sequence in which they occur we now know
  • 00:05:03
    that a.d begins with clinically silent
  • 00:05:05
    processes which lead to the appearance
  • 00:05:08
    of symptoms decades later diagnosis of
  • 00:05:11
    the earliest stages of ad is being aided
  • 00:05:13
    by emerging risk factor evidence
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    improved screening tools that evaluate
  • 00:05:18
    symptoms with greater accuracy and novel
  • 00:05:20
    techniques for the detection and
  • 00:05:22
    measurement of ad biomarkers
  • 00:05:25
    it is hoped that ongoing and future
  • 00:05:27
    research continues to help unravel the
  • 00:05:29
    causes of ad
  • 00:05:31
    and hopefully aids in better treatment
  • 00:05:33
    of this complex disease
  • 00:05:36
    [Music]
  • 00:06:02
    you
タグ
  • Alzheimer
  • ziekte
  • symptomen
  • diagnose
  • biomarkers
  • behandelingen
  • neurologie
  • neurodegeneratie
  • tau-eiwit
  • a bèta