Pathophysiology of Alzheimer's disease (AD) yɛ ade a ɛkyere adwene a ɛhwehwɛ sɛ protein a enni mu boaboa ano, ahohyehye, ne amemene mu yare.
Nneɛma atitiriw abien a ɛma yehu sɛ obi anya AD ne amyloid-beta (Aβ) ntontom ne ntini a ɛbom yɛ adwuma wɔ amemene no mu.
Amyloid-beta plaques nya ne nnyinasoɔ bere a enzymes paapae amyloid precursor protein (APP) mu ma ɛyɛ Aβ peptides.
Saa peptide yi boa ano ma ɛyɛ fibril a wontumi nhye mu ma ɛboaboa ano wɔ amemene no akyi, na ɛsɛe nkwammoaa nkitahodie a ɛda wɔn ntam no ma amemene no wu.
Wosusuw sɛ Aβ ntɛtɛ a ɛboaboa ano no yɛ ade a edi kan a ɛde AD ba, na wogye di sɛ ɛde ba wɔ amemene mu yare no mu.
Neurofibrillary tangles no yɛ bere a protein tau no nya ahoɔden ma ɛbɔ abnormalities wɔ neuron mu.
Saa ntontan yi sɛe adwuma a microtubules yɛ no, na ɛho hia ma nnuannuru ne nneɛma foforo a ɛkɔ amemene no mu.
Awiei koraa no, ntini a akeka bom no ma amemene no wu.
Sɛ yareɛ no bɔ obi a, na ɛyɛ yareɛ a ɛde yare ba.
Nipadua mu nkwaadɔm no ko tia mmoawa a wɔboa ma nipadua no ko tia nyarewa no denam cytokine a ɛma nipadua no ko tia nyarewa no a ebetumi asɛe amemene no mu.
Bio nso, adanseɛ kyerɛ sɛ adwennwene a ɛde mframa ba nipadua mu, mitochondrial dysfunction, ne glucose a wɔde di dwuma wɔ nipadua mu no nso ka ho bi na ɛma AD ba.
Saa nneɛma yi betumi ama amemene no asɛe na ama awu, na ama yare no mu ayɛ den kɛse.
Ne nyinaa mu no, AD yare no yɛ nneɛma pii a ɛka bom ma adwene a obi kura so tew na ne werɛ fi ade.
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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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