Alzheimer yare no yɛ yare a ɛyɛ den a ɛma mogya mu ahoɔdennuru pii tu fra, na ɛma nipadua no yɛ basaa.
Nneɛma atitiriw abien a ɛma obi nya AD ne amyloid-beta (Aβ) ntokuru ne ntokuru a ɛkyere adwene (NFT) a ɛwɔ amemene no mu.
Sɛ nnuru a ɛma nipadua no nya ahoɔden no tumi ma amyloid-beta plaque no so tew a, ɛma wonya Aβ peptide.
Saa peptide yi bom yɛ ntini a wontumi nkan a ɛboaboa ano wɔ amemene no mu, na ɛsɛe nkwammoaa nkitahodi ma amemene no wu.
Wosusuw sɛ Aβ ntokuru a ɛboaboa ano no yɛ ade a edi kan a ɛma AD ba, na wogye di sɛ ɛde ba.
Neurofibrillary twitwiw twitwiw bere a protein tau no nya ahoɔden kɛse ma ɛyɛ ntini a enni mu wɔ amemene mu no.
Saa ntokuru yi sɛe adwuma a nkwammoaa nketenkete a ɛboa ma nkwammoaa no nya nnuannuru ne nneɛma foforo no yɛ no.
Awiei koraa no, nkwammoaa a ɛreyɛ adwuma no wu.
Ntini mu yare nso ka ho bi na AD ba.
Na nipadua mu tumi a ɛko tia nyarewa no de nkwammoaa mu yare a ɛde yare ba no ba mu.
Bio nso, adanse wɔ hɔ a ɛkyerɛ sɛ adwennwene a ɛma nipadua no wosow ahoɔden, mitochondrial a ɛmma adwuma nyɛ yiye, ne glucose a wonnya no ma obi nya AD.
Saa nneɛma yi betumi ama amemene no mu ayɛ adwuma yiye na awu, na ama yare no mu ayɛ den kɛse.
Ne nyinaa mu no, AD yare no ho ade a ɛma obi tumi hu ade yiye ne sɛnea ne werɛ fi ade no yɛ nneɛma pii a ɛka bom ma ɛhaw adwene.
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.
['Nsɛm a Ɛnsɛ sɛ Wɔka:']
['Wɔayɛ wɛbsaet yi sɛ wɔmfa nkyerɛkyerɛ na wɔmfa nkyerɛkyerɛ afoforo, na ɛnyɛ sɛ wɔde rema aduruyɛ ho afotu anaa wɔde rema adwuma.']
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['Yɛsrɛ wo hyɛ no nsow sɛ, sɛnea wɔhwɛ nsɛmmisa no so no, sɛ ɛba sɛ wɔrekyerɛw nnipa dodow a wɔanya yare bi ho asɛm a, ɛntaa nsi yiye.']
['Hwehwɛ afotu fi wo duruyɛfo anaa ɔyaresafo foforo a ɔfata hɔ bere biara wɔ yare bi ho. Nnya adwene sɛ wo nsa bɛka oduruyɛfo afotu anaasɛ wubetwa so esiane biribi a woakenkan wɔ wɛbsaet yi so nti. Sɛ wususuw sɛ ebia wo ho behia wo wɔ ayaresa mu a, frɛ 911 anaa kɔ ayaresabea a ɛbɛn wo paa ntɛm ara.']
['Nsɛm a wɔmmɔ ho ban:']
['Digital Millennium Copyright Act a wɔhyɛe wɔ afe 1998 mu, 17 U.S.C. § 512 (DMCA) no ma wɔn a wɔwɔ hokwan sɛ wɔyɛ wɔn nneɛma no kwan sɛ wɔyɛ nea wɔpɛ biara.']
["Sɛ wugye di sɛ nsɛm anaa nneɛma a ɛwɔ yɛn wɛbsaet anaa yɛn dwumadibea no mu bi to wo mmara a wode bɔɔ nneɛma ho ban no a, wo (anaa w'ananmusifo) betumi de krataa akɔma yɛn de aka sɛ yɛnyi nsɛm anaa nneɛma no, anaa yɛmmɔ kwan mma wonnya bi."]
["Ɛsɛ sɛ wɔde krataa ne email na ɛbɔ amanneɛ (hwɛ 'Contact' afã hɔ na wubehu email address)."]
['DMCA hwehwɛ sɛ wo amanneɛbɔ a ɛfa nea wɔkyerɛ sɛ ɛyɛ mmara a wobu so ho no de nsɛm a edidi so yi ka ho: (1) adwuma a mmara bɔ ho ban a wɔkyerɛ sɛ wɔadi so no ho asɛm; (2) nsɛm a wɔkyerɛ sɛ wɔadi so no ho asɛm ne nsɛm a ɛbɛboa yɛn ma yɛahu baabi a ɛwɔ; (3) wo ho nsɛm a yɛde bedi nkitaho, a wo address, telefon nɔma ne email address ka ho; (4) wo nsɛm a ɛkyerɛ sɛ wugye di sɛ nea wɔabɔ ho sobo no nyɛ nea mmara ma ho kwan; ']
['(5) wo nsahyɛ a ɛkyerɛ sɛ nsɛm a ɛwɔ amanneɛbɔ no mu yɛ nokware, na wowɔ tumi sɛ wode nea wɔkyerɛ sɛ woadi ho dwuma no bedi dwuma; ']
['ne (6) nea ɔwɔ tumi sɛ ɔyɛ biribi ma obi a ɔwɔ tumi sɛ ɔyɛ biribi ma no no nsaano nkyerɛwee.']
['Sɛ woamfa nsɛm a yɛaka yi nyinaa anka ho a, ebetumi ama wo ka no akyɛ.']
['Nkitahodi']
['Yɛsrɛ wo, fa nsɛmmisa anaa nyansahyɛ biara a wowɔ brɛ yɛn wɔ e-mail so.']
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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