De pathofysiologie vaan de ziekte vaan Alzheimer (AD) is 'n complex proces boebij abnormale proteïne, ontsteking en neuronale disfunctie ophoop.
De twie hoofkenmerke vaan AD zien de aonwezigheid vaan amyloid-beta (Aβ) plaques en neurofibrillary tangles (NFTs) in de hersene.
Amyloid-beta plaques weure gevörmp es fragmente vaan 't amyloid-precursor-eiwit (APP) door enzymen weure gesplete um Aβ-peptide te vörme.
Dees peptide aggregere en vörme onoplosbare fibrille die zich ophoupe boete neurone, wat de communicatie vaan cel tot cel verangert en tot neuronaole doed leidt.
De opeenhoping vaan Aβ-plaques is ein vaan de ierste gebeurtenisse in de oontwikkeling vaan AD, en heet 'n bijdrage aon 't neurodegeneratief perces.
Neurofibrillaire klitten weure gevörmp es 't proteïne tau hyperfosforyleert en abnormale filamente binne neurone vörmp.
Dees verwikkelinge verstoore de normale wirking vaan de microtubuli, die essentieel zien veur 't transport vaan voedingstowwe en ander materiaole binne 't neuron.
De wirkzaamheid vaan de neurone is sterk versjèlle.
De ontsteking speult ouch 'n rol in de pathofysiologie vaan AD.
't Immuunsysteem reageert op de opeenhoping vaan Aβ-plaques en NFT's door pro-inflammatoire cytokines vrij te geve, die de sjaoj aon neurone kinne verergerere.
Daoneve is d'r bewies det oxidatieve stress, mitochondriale disfunctie en verangerde glucose metabolisme bijdrage aon de pathofysiologie vaan AD.
Dees factore kinne leije tot neuronale disfunctie en doed, wat 't krenkdeperces nog vererger.
De pathofysiologie vaan de ziekte vaan Alzheimer is 'n complex samewèrking vaan väölfactoren die oeteindelek leije tot de progressieve achteruitgaank vaan de cognitieve functie en geheugeverlies wat de krenkde kinmerkt.
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What is pathophysiology of alzheimer?
The pathophysiology of Alzheimer's disease (AD) is a complex process that involves the accumulation of abnormal proteins, inflammation, and neuronal dysfunction.
The two main hallmarks of AD are the presence of amyloid-beta (Aβ) plaques and neurofibrillary tangles (NFTs) in the brain.
Amyloid-beta plaques are formed when fragments of the amyloid precursor protein (APP) are cleaved by enzymes to form Aβ peptides.
These peptides aggregate and form insoluble fibrils that accumulate outside neurons, disrupting cell-to-cell communication and leading to neuronal death.
The accumulation of Aβ plaques is thought to be one of the earliest events in the development of AD, and it is believed to contribute to the neurodegenerative process.
Neurofibrillary tangles are formed when the protein tau becomes hyperphosphorylated and forms abnormal filaments inside neurons.
These tangles disrupt the normal functioning of the microtubules, which are essential for the transport of nutrients and other materials within the neuron.
The tangles eventually lead to the death of the affected neurons.
Inflammation also plays a role in the pathophysiology of AD.
The immune system responds to the accumulation of Aβ plaques and NFTs by releasing pro-inflammatory cytokines, which can exacerbate the damage to neurons.
Additionally, there is evidence that oxidative stress, mitochondrial dysfunction, and impaired glucose metabolism contribute to the pathophysiology of AD.
These factors can lead to neuronal dysfunction and death, further exacerbating the disease process.
Overall, the pathophysiology of AD is a complex interplay of multiple factors that ultimately lead to the progressive decline in cognitive function and memory loss that characterizes the disease.
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