Il- patofiżjoloġija tal- marda ta ' Alzheimer (AD) hija proċess kumpless li jinvolvi l- akkumulazzjoni ta ' proteini anormali, infjammazzjoni, u disfunzjoni newronali.
Iż- żewġ karatteristiċi ewlenin taʼ AD huma l- preżenza taʼ plaċċi taʼ amyloid- beta (Aβ) u taʼ neurofibrillary tangles (NFTs) fil- moħħ.
Il- plaċi tal- amilojdi- beta jiffurmaw meta frammenti tal- proteina prekursur tal- amilojdi (APP) jinqasmu mill- enżimi biex jiffurmaw peptidi Aβ.
Dawn il- peptidi jingħaqdu u jiffurmaw fibrilli insolubbli li jakkumulaw barra n- newroni, u jfixklu l- komunikazzjoni bejn iċ- ċelloli u jwasslu għall- mewt newronali.
L- akkumulazzjoni ta ' plaċi Aβ hija meqjusa bħala waħda mill- ewwel avvenimenti fl- iżvilupp ta ' AD, u huwa maħsub li tikkontribwixxi għall- proċess newrodegenerattiv.
Il- tangles neurofibrillari jiffurmaw meta l- proteina tau ssir iperfosforilata u tifforma filamenti anormali ġewwa n- newroni.
Dawn il- ħbula jfixklu l- funzjonament normali tal- mikrotubuli, li huma essenzjali għat- trasport taʼ nutrijenti u materjali oħra ġewwa n- newron.
L- infjammazzjoni għandha wkoll rwol fil- patofiżjoloġija tal- AD.
Is- sistema immunitarja tirrispondi għall- akkumulazzjoni ta ' plaċi Aβ u NFTs billi tirrilaxxa ċitokini pro- infjammatorji, li jistgħu jħaffu l- ħsara lin- newroni.
Barra minn hekk, hemm evidenza li l- stress ossidattiv, id- disfunzjoni mitokondrijali, u l- metaboliżmu tal- glukożju mfixkel jikkontribwixxu għall- patofiżjoloġija ta ' AD.
Dawn il- fatturi jistgħu jwasslu għal disfunzjoni newronali u mewt, li jkompli jħaffer il- proċess tal- marda.
B'mod ġenerali, il- patofiżjoloġija ta ' AD hija interazzjoni kumplessa ta ' fatturi multipli li fl- aħħar mill- aħħar iwasslu għal tnaqqis progressiv fil- funzjoni konjittiva u telf ta ' memorja li jikkaratterizza l- marda.
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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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