Patofisiologi penyakit Alzheimer (AD) minangka proses kompleks sing kalebu akumulasi protein abnormal, peradangan, lan disfungsi neuron.
Loro ciri khas utama AD yaiku anané plak amiloid-beta (Aβ) lan tangles neurofibrillary (NFTs) ing otak.
Plak amiloid-beta dibentuk nalika fragmen protein prekursor amiloid (APP) dipecah dening enzim kanggo mbentuk peptida Aβ.
Peptida kasebut nglumpukake lan mbentuk fibril sing ora larut sing nglumpukake ing njaba neuron, ngganggu komunikasi sel-sel lan nyebabake pati neuron.
Akumulasi plak Aβ dianggep minangka salah sawijining acara paling awal ing pangembangan AD, lan dipercaya nyumbang kanggo proses neurodegeneratif.
Tangles neurofibrillary dibentuk nalika protein tau dadi hyperphosphorylated lan mbentuk filamen abnormal ing njero neuron.
Gangguan kasebut ngganggu fungsi normal mikrotubulus, sing penting kanggo transportasi nutrisi lan bahan liyane ing neuron.
Genggeman kasebut pungkasane nyebabake pati neuron sing kena pengaruh.
Peradangan uga duwe peran ing patofisiologi AD.
Sistem kekebalan awak nanggapi akumulasi plak Aβ lan NFT kanthi ngeculake sitokin pro-inflamasi, sing bisa nambah karusakan neuron.
Kajaba iku, ana bukti manawa stres oksidatif, disfungsi mitokondria, lan metabolisme glukosa sing rusak nyumbang kanggo patofisiologi AD.
Faktor-faktor kasebut bisa nyebabake disfungsi neuron lan pati, luwih nggedhekake proses penyakit.
Sakabèhé, patofisiologi AD minangka interaksi kompleks saka pirang-pirang faktor sing pungkasane nyebabake penurunan progresif ing fungsi kognitif lan mundhut memori sing nggambarake penyakit kasebut.
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Casadesus G, Moreira PI, Nunomura A, Siedlak SL, Bligh-Glover W, Balraj E, Petot G, Smith MA, Perry G: Indices of metabolic dysfunction and oxidative stress. Neurochem Res. , 32 (4-5): 717-22.
Candore G, Bulati M, Caruso C, Castiglia L, Colonna-Romano G, Di Bona D, Duro G, Lio D, Matranga D, Pellicanò M, Rizzo C, Scapagnini G, Vasto S: Inflammation, cytokines, immune response, apolipoprotein E, cholesterol, and oxidative stress in Alzheimer disease: therapeutic implications. Rejuvenation Res. , 13 (2-3): 301-13.
Schindler SE, McConathy J, Ances BM, Diamond MI: Advances in diagnostic testing for Alzheimer disease. Mo Med. , 110 (5): 401-5.
Singh VK: Immune-activation model in Alzheimer disease. Mol Chem Neuropathol. , 28 (1-3): 105-11.
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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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