Pathophysiology ea lefu la Alzheimer (AD) ke mokhoa o rarahaneng o akarelletsang ho bokellana ha liprotheine tse sa tloaelehang, ho ruruha le ho se sebetse hantle ha methapo ea kutlo.
Matšoao a mabeli a ka sehloohong a lefu la Alzheimer ke ho ba teng ha li-plaque tsa amyloid-beta (Aβ) le li-neurofibrillary tangles (NFT) bokong.
Li-plaque tsa amyloid-beta li thehoa ha likarolo tsa protheine ea amyloid precursor (APP) li qhaqhoa ke li-enzyme hore li etse li-peptide tsa Aβ.
Li-peptide tsena lia kopana'me li etsa li-fibril tse sa qhibilihang tse bokellanang ka ntle ho methapo ea kutlo, li sitisa puisano ea sele le sele'me li etsa hore methapo ea kutlo e shoe.
Ho nahanoa hore ho bokellana ha li-plaque tsa Aβ ke e 'ngoe ea liketsahalo tsa pele-pele tse bakang lefu la Alzheimer,' me ho lumeloa hore ho tlatsetsa ho senyeheng ha methapo ea kutlo.
Ho thehoa li-tangle tsa li-neurofibrillary ha protheine ea tau e fetoha hyperphosphorylated'me e etsa likhoele tse sa tloaelehang ka har'a li-neuron.
Lintho tsena tse rarahaneng li sitisa tšebetso e tloaelehileng ea li-microtubule, tse hlokahalang bakeng sa ho tsamaisa limatlafatsi le lintho tse ling ka har'a neuron.
Qetellong, ho rarahana ha lisele tsena ho etsa hore li shoe.
Ho ruruha ho boetse ho phetha karolo ho pathophysiology ea AD.
Tsamaiso ea'mele ea ho itšireletsa mafung e arabela ho bokelleng ha li-plaque tsa Aβ le li-NFT ka ho lokolla li-cytokine tse susumetsang ho ruruha, tse ka mpefatsang tšenyo ea methapo ea kutlo.
Ho phaella moo, ho na le bopaki ba hore khatello ea mali, ho se sebetse hantle ha mitochondrial le ho senyeha ha metabolism ea tsoekere ho tlatsetsa ho pathophysiology ea AD.
Lintho tsena li ka etsa hore methapo ea kutlo e se ke ea sebetsa hantle'me ea shoa, e leng se mpefatsang lefu lena le ho feta.
Ka kakaretso, pathophysiology ea AD ke tšebelisano e rarahaneng ea lintho tse ngata tse qetellang li lebisa ho fokotseheng ho tsoelang pele ha ts'ebetso ea kelello le tahlehelo ea mohopolo e khethollang lefu lena.
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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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