Pathophysiology ya bolwetse jwa Alzheimer (AD) ke thulaganyo e e raraaneng e e akaretsang go koelana ga diporoteine tse di sa tlwaelegang, go ruruga le go sa dire sentle ga ditshika tsa boboko.
Matshwao a mabedi a konokono a bolwetse jwa Alzheimer ke go nna gone ga plaque ya amyloid-beta (Aβ) le neurofibrillary tangles (NFTs) mo bobokong.
Amyloid-beta plaques e bopiwa fa dikarolwana tsa amyloid precursor protein (APP) di kgaoganngwa ke di-enzyme go bopa di-Aβ peptide.
Di-peptide tseno di a kopana di bo di dira di-fibril tse di sa tlhaoleng tse di kgobokanang ka kwa ntle ga di-neuron, di kgoreletsa puisano ya sele le sele mme di bo di dira gore di-neuron di swe.
Go akanngwa gore go koelana ga plaque ya Aβ ke sengwe sa dilo tsa ntlha tse di bakang bolwetse jwa Alzheimer, mme go akanngwa gore go ka baka bolwetse jwa boboko.
Neurofibrillary tangles di bopega fa poroteine tau e nna hyperphosphorylated mme e bo e bopa ditlhale tse di sa tlwaelegang mo teng ga di-neuron.
Ditlhatshana tseno di kgoreletsa tsela e di-microtubule di berekang ka yone, tse di botlhokwa thata mo go tsamaiseng dikotla le dilo tse dingwe mo teng ga nyurone.
Kgabagare go raraana gono go dira gore dinyurone tse di amilweng di swe.
Go ruruga gape go na le seabe mo pathophysiology ya Alzheimer.
Thulaganyo ya mmele ya go lwantsha malwetse e tsibogela go kgobokana ga di-Aβ plaque le di-NFT ka go ntsha di-cytokine tse di bakang go ruruga, tse di ka gakatsang tshenyo ya di-neurons.
Mo godimo ga moo, go na le bosupi jwa gore go ngomoga pelo ka ntlha ya okosejene, go sa dire sentle ga mitochondrial, le go sa dire sentle ga glucose metabolism di dira gore motho a nne le bolwetse jwa Alzheimer.
Dilo tseno di ka dira gore ditshika tsa boboko di se ka tsa bereka sentle le go swa, mme seo se gakatsa bolwetse.
Ka kakaretso, pathophysiology ya bolwetse jwa Alzheimer ke tsela e e raraaneng e dilo di le dintsi di dirisanang ka yone e kgabagare e dirang gore motho a nne le bothata jwa go sa kgone go akanya sentle le go latlhegelwa ke mogopolo.
Nemeroff CB: The preeminent role of neuropeptide systems in the early pathophysiology of Alzheimer disease: up with corticotropin-releasing factor, down with acetylcholine. Arch Gen Psychiatry. 1999, 56 (11): 991-2.
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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