Is próiseas casta é pathophysiology galar Alzheimer (AD) a chuimsíonn carnadh próitéiní neamhghnácha, athlasadh, agus mífheidhmiú néarónach.
Is iad an dá phríomhghné de AD ná láithreacht plaic amyloid-beta (Aβ) agus tangles neurofibrillary (NFTs) sa inchinn.
Cruthaítear plaicí amyloid-beta nuair a scriosann einsímí codanna den próitéin réamhtheachtaí amyloid (APP) chun peptides Aβ a fhoirmiú.
Déantar na peiptídeanna seo a chruinniú agus a fhoirmiú fibrils neamhshláintiúla a chruinníonn lasmuigh de na néaróin, ag cur isteach ar chumarsáid cealla-go-chealla agus a fhágann go bhfaigheann néaróin bás.
Meastar go bhfuil carnadh plaic Aβ ar cheann de na himeachtaí is luaithe i bhforbairt AD, agus creidtear go gcuireann sé leis an bpróiseas néareodegenerative.
Cruthaítear tangles neurofibrillary nuair a bhíonn an próitéin tau hyperphosphorylated agus cruthaíonn sé filaments neamhghnácha taobh istigh de néaróin.
Cuireann na tangles seo isteach ar fheidhmiú gnáth na microtubules, atá riachtanach chun cothaithigh agus ábhair eile a iompar laistigh den neuróin.
Mar thoradh ar na tangles sa deireadh báis na néaróin a bhfuil tionchar acu orthu.
Tá ról ag athlasadh freisin i pathophysiology AD.
Freagraíonn an córas imdhíonachta ar chruinnithe plaic Aβ agus NFTs trí cytokines pro-inflammatory a scaoileadh, rud a d'fhéadfadh damáiste a dhéanamh do néaróin a mhéadú.
Ina theannta sin, tá fianaise ann go gcuireann strus ocsaídiúil, mífheidhmiú mitochondrial, agus meitibileacht glúcóis laghdaithe le pathophysiology AD.
D'fhéadfadh na fachtóirí seo a bheith ina chúis le mífheidhmiú néarónach agus le bás, rud a mhéadaíonn an próiseas galair tuilleadh.
Ar an iomlán, is idirghníomhaíocht chasta de fhachtóirí iomadúla é pathophysiology AD a fhágann sa deireadh an titim forásach ar fheidhm chognaíoch agus caillteanas cuimhne a shainaithníonn an galar.
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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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