Pathophysiology panyakit Alzheimer (AD) nyaéta prosés nu kompléks nu ngalibatkeun akumulasi protéin abnormal, peradangan, jeung disfungsi neuron.
Dua ciri utama Alzheimer nyaéta ayana plak béta-amiloid (Aβ) jeung neuron-fibrillary tangles (NFT) dina uteuk.
Plak béta-amiloid kabentuk lamun fragmen protéin prékursor béta-amiloid (APP) dibeulah ku énzim pikeun ngabentuk péptida Aβ.
Péptida ieu ngagabung jeung ngabentuk serat nu teu leyur nu ngumpul di luar neuron, ngaruksak komunikasi sél-ka-sél sarta ngabalukarkeun maot neuron.
Akumulasi plak Aβ dianggap salah sahiji kajadian pangheulana dina ngembangkeun AD, sarta dipercaya nyumbang kana prosés neurodegeneratif.
Neurofibrillary tangles kabentuk nalika protéin tau jadi hyperphosphorylated sarta ngabentuk filamén abnormal dina jero neuron.
Ieu tangles ngaruksak fungsi normal tina mikrotubulus, nu penting pikeun ngangkut gizi jeung bahan séjénna dina neuron.
Ku kituna, neuron nu kaganggu bakal maot.
Peradangan ogé boga peran dina patofisiologi Alzheimer.
Sistem imun ngaréspon akumulasi plak Aβ jeung NFT ku ngaleupaskeun sitokin pro-radang, nu bisa ngagedékeun karuksakan neuron.
Salian ti éta, aya bukti yén stress oksidatif, disfungsi mitokondria, jeung gangguan métabolisme glukosa ogé ngabalukarkeun panyakit Alzheimer.
Faktor-faktor ieu bisa ngabalukarkeun disfungsi jeung maotna neuron, nu bisa ngagedékeun panyakit.
Sacara umum, patofisiologi Alzheimer mangrupa interaksi nu kompleks tina sababaraha faktor nu ahirna ngabalukarkeun kamunduran fungsi kognitif jeung leungitna ingetan nu jadi ciri panyakit ieu.
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Proft J, Weiss N: Jekyll and Hide: The two faces of amyloid β. Commun Integr Biol. 2012, 5 (5): 405-7.
Whitehouse PJ, Hedreen JC, White CL, Price DL: Basal forebrain neurons in the dementia of Parkinson disease. Ann Neurol. 1983, 13 (3): 243-8.
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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