Alzheimer yare yɛ yare a ɛma obi adwene yɛ adwuma yiye a edi kan nya adwene no so nkɛntɛnso, na ɛma obi werɛ fi nneɛma, n'adwene yɛ adwuma yiye, na ɔyɛ nneɛma bi a ɛmfata.
Wɔnte nea ɛde Alzheimer yare no ba no ase yiye, nanso wogye di sɛ efi awosu, nneɛma a atwa yɛn ho ahyia, ne asetra kwan mu.
Nneɛma a ebetumi ama obi anya Alzheimer yare no bi ne:
1. Abusuasɛm: Wɔahu awosu bi a ɛma obi nya Alzheimer yare no, titiriw awosu a ɛma obi nya apolipoprotein E (APOE) no.
2. Mfe a obi adi: Sɛ obi nyin a, ɛyɛ den sɛ obenya Alzheimer yare no, na nnipa dodow no ara nya bi bere a wɔadi mfe 65 akyi.
3. Abusua mu abakɔsɛm: Sɛ obi abusua mufo anya Alzheimer yare no bi a, ebetumi ama yare no a ɛbɛba no ayɛ kɛse.
4. Ti a wopirapira: Sɛ obi apira ne ti pɛn, titiriw nea ɛma n'ani so tetew no a, ebetumi ama wanya Alzheimer yare no bi.
5. Komayare: Nyarewa te sɛ mogya mmoroso, mogya mu srade pii, ne asikreyare betumi ama obi anya Alzheimer yare.
6. Asetra kwan: Sɛ obi tra ase kyɛ, odi aduan a ahoɔden nnim, na n'adwene nyɛ adwuma yiye a, ebetumi ama wanya Alzheimer yare no bi.
7. Ntini a ɛrehyew: Ntini a ɛrehyew wɔ amemene mu no betumi ama obi anya Alzheimer yare.
8. Adwennwen a ɛma nipadua no yɛ mmerɛw: Sɛ nipadua no ntumi nyi awuduru mfi nipadua no mu sɛnea ɛsɛ a, ebetumi ama obi anya Alzheimer yare.
9. Amyloid ntokuru ne ntokuru a ɛkyekyere adwene: Ntokuru a ɛkyekyere adwene ne ntokuru a ɛkyekyere adwene a ɛboaboa ano wɔ amemene no mu no yɛ Alzheimer yare no ho sɛnkyerɛnne, nanso wɔnte dwuma a wodi wɔ yare no mu no ase nwie.
Ɛho hia sɛ yɛhyɛ no nsow sɛ Alzheimer yare no ho nsɛm dɔɔso na ebetumi aba sɛ saa nneɛma yi nyinaa ka ho.
Wɔreyɛ nhwehwɛmu akɔ akyiri na ama wɔahu nea ɛde ba na wɔanya aduru a ɛbɛboa yare a ɛyɛ hu yi.
Vellas B, Andrieu S, Cantet C, Dartigues JF, Gauthier S: Long-term changes in ADAS-cog: what is clinically relevant for disease modifying trials in Alzheimer? J Nutr Health Aging. , 11 (4): 338-41.
Braak E, Griffing K, Arai K, Bohl J, Bratzke H, Braak H: Neuropathology of Alzheimer's disease: what is new since A. Alzheimer? Eur Arch Psychiatry Clin Neurosci. 1999, 249 Suppl 3 (): 14-22.
Kovacs GG: Can Creutzfeldt-Jakob disease unravel the mysteries of Alzheimer? Prion. 2016, 10 (5): 369-376.
Cankurtaran M, Yavuz BB, Cankurtaran ES, Halil M, Ulger Z, Ariogul S: Risk factors and type of dementia: vascular or Alzheimer? Arch Gerontol Geriatr. , 47 (1): 25-34.
Mahami-Oskouei M, Hamidi F, Talebi M, Farhoudi M, Taheraghdam AA, Kazemi T, Sadeghi-Bazargani H, Fallah E: Toxoplasmosis and Alzheimer: can Toxoplasma gondii really be introduced as a risk factor in etiology of Alzheimer? Parasitol Res. 2016, 115 (8): 3169-74.
['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.']
['Ɛnsɛ sɛ wɔde nsɛm a wɔde ama no di dwuma de hwehwɛ yare bi ho yare anaa wɔde sa yare, na ɛsɛ sɛ wɔn a wɔrehwehwɛ ayaresa ho afotu no kohu oduruyɛfo a ɔwɔ tumi krataa.']
['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 causes alzheimer?
Alzheimer's disease is a progressive neurodegenerative disorder that primarily affects the brain, causing memory loss, cognitive decline, and behavioral changes.
The exact cause of Alzheimer's disease is not fully understood, but it is believed to result from a combination of genetic, environmental, and lifestyle factors.
Some of the factors that may contribute to the development of Alzheimer's disease include:
1. Genetics: Certain genes have been identified that increase the risk of developing Alzheimer's disease, particularly the apolipoprotein E (APOE) gene.
2. Age: The risk of developing Alzheimer's disease increases with age, with most people being diagnosed after the age of 65.
3. Family history: Having a family history of Alzheimer's disease may increase the risk of developing the condition.
4. Head injuries: A history of head injuries, particularly those that result in loss of consciousness, may increase the risk of Alzheimer's disease.
5. Cardiovascular risk factors: Conditions such as high blood pressure, high cholesterol, and diabetes may increase the risk of developing Alzheimer's disease.
6. Lifestyle factors: A sedentary lifestyle, poor diet, and lack of mental stimulation may increase the risk of Alzheimer's disease.
7. Inflammation: Chronic inflammation in the brain may contribute to the development of Alzheimer's disease.
8. Oxidative stress: An imbalance between the production of free radicals and the body's ability to detoxify them may contribute to the development of Alzheimer's disease.
9. Amyloid plaques and neurofibrillary tangles: The accumulation of amyloid plaques and neurofibrillary tangles in the brain is a hallmark of Alzheimer's disease, but the role they play in the development of the condition is not fully understood.
It is important to note that the cause of Alzheimer's disease is complex and likely involves a combination of these factors.
Research is ongoing to better understand the underlying mechanisms and develop effective treatments for this devastating condition.
Disclaimer: medical
This web site is provided for educational and informational purposes only and does not constitute providing medical advice or professional services.
The information provided should not be used for diagnosing or treating a health problem or disease, and those seeking personal medical advice should consult with a licensed physician.
Please note the neural net that generates answers to the questions, is specially inaccurate when it comes to numeric content. For example, the number of people diagnosed with a specific disease.
Always seek the advice of your doctor or other qualified health provider regarding a medical condition. Never disregard professional medical advice or delay in seeking it because of something you have read on this website. If you think you may have a medical emergency, call 911 or go to the nearest emergency room immediately. No physician-patient relationship is created by this web site or its use. Neither BioMedLib nor its employees, nor any contributor to this web site, makes any representations, express or implied, with respect to the information provided herein or to its use.
Disclaimer: copyright
The Digital Millennium Copyright Act of 1998, 17 U.S.C. § 512 (the “DMCA”) provides recourse for copyright owners who believe that material appearing on the Internet infringes their rights under U.S. copyright law. If you believe in good faith that any content or material made available in connection with our website or services infringes your copyright, you (or your agent) may send us a notice requesting that the content or material be removed, or access to it blocked. Notices must be sent in writing by email (see 'Contact' section for email address) . The DMCA requires that your notice of alleged copyright infringement include the following information: (1) description of the copyrighted work that is the subject of claimed infringement; (2) description of the alleged infringing content and information sufficient to permit us to locate the content; (3) contact information for you, including your address, telephone number and email address; (4) a statement by you that you have a good faith belief that the content in the manner complained of is not authorized by the copyright owner, or its agent, or by the operation of any law; (5) a statement by you, signed under penalty of perjury, that the information in the notification is accurate and that you have the authority to enforce the copyrights that are claimed to be infringed; and (6) a physical or electronic signature of the copyright owner or a person authorized to act on the copyright owner’s behalf. Failure to include all of the above information may result in the delay of the processing of your complaint.
['Ɛfa ho']
['BioMedLib de kɔmputa a wɔde di dwuma (mfidie a wɔde sua ade) na ɛma nsɛmmisa ne mmuae.']
['Yɛde nhoma ahorow a ɛfa nnuruyɛ mu ɔpepem 35 a ɛwɔ PubMed/Medline ne RefinedWeb mu na efii ase.']
