Patofisiologi panyakik Alzheimer (AD) adolah proses kompleks nan maliputi akumulasi protein abnormal, radang, jo disfungsi neuronal.
Kaduo ciri utamo panyakik Alzheimer adolah adonyo plak amiloid-beta (Aβ) jo neurokabel (NFT) di utak.
Plak amiloid-beta tabantuak katiko pacahan protein pendahulu amiloid (APP) dipacah dek enzim untuak mambantuak peptida Aβ.
Peptida iko mangumpua jo mambantuak fibril nan indak laruik nan mangumpuakan di lua neuron, mangacaukan komunikasi sel-sel jo manyababkan kamatian neuron.
Akumulasi plak Aβ dianggap sabagai salah satu kajadian nan paliang awa dalam parkambangan AD, dan diyakini dapek manyumbang pado proses neurodegeneratif.
Tali-tali neurofibrillary tabantuak katiko protein tau manjadi hiperfosforilasi jo mambantuak filamen abnormal di dalam neuron.
Tali-tali iko mangacaukan fungsi normal mikrotubulus, nan pantiang untuak transportasi nutrisi jo bahan lain di dalam neuron.
Pangkaik-angkaik akhianyo manyababan kamatian neuron nan taserak.
Radang juo baparan dalam patofisiologi AD.
Sistem kakebalan mananggapi akumulasi plak Aβ jo NFT jo malapehan sitokin pro-inflamasi, nan dapek maningkekan karusakan neuron.
Salain itu, ado bukti baso stres oksidatif, disfungsi mitokondria, jo gangguan metabolisme glukosa dapek manyababkan panyakik Alzheimer.
Faktor-faktor iko dapek manyababkan disfungsi jo kamatian neuron, nan labiah maningkekkan panyakik.
Sacaro kasaluruahan, patofisiologi AD adolah interaksi kompleks dari babagai faktor nan akhianyo manyababan panurunan progresif fungsi kognitif jo hilangnyo ingatan nan manjadi ciri panyakik ko.
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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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