Patofisiologi Alzheimer Disease

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PATOFISIOLOGI AD Anggraeni Parwati (04) Kelompok 9 09-036

Transcript of Patofisiologi Alzheimer Disease

Page 1: Patofisiologi Alzheimer Disease

PATOFISIOLOGI ADAnggraeni Parwati (04)Kelompok 909-036

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Letak anatomis

•Hipokampus•Korteks temporal•Nukleus basalis

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Mikroskopis

• Ditemukan :

▫ Senile plaque

▫ Neurofibrilles tangles (NFTs)

• Proses degeneratif normal, terakumulasi kecil di

hipokampus.

• Inti pusat senile plaque mengandung β-amyloid,

proteoglikan, Apo 4, 1 antichymotrypsin & protein lainnya.

• Dikeliling inti plaque terdapat degenrasi neuron, mikroglia

& makrofag.

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Mikroskopis

• β-amyloid : protein yg tdd 39-42 as.amino yg

merupakan turunan dari amyloid precursor protein

(APP).

• APP memiliki fungsi neurotropik dan neuroprotektif.(enzim γ dan β sekretase)

APP β-amyloid

• Fibril amyloid terlarut disebut oligomer.

Akumulasinya senile plaque.

• Gagal melipatnya molekul A42 zat paling beracun

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Mikroskopis

• NFTs : sepasang neurofilamen di dalam

sitoplasma neuron & merupakan protein τ

terfosforilasi dlm jml byk.

• τ berfungsi membentuk & menstabilkan

mikrotubulus yang membawa sel organel,

glikoprotein & lainnya.

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Neurotransmitters

• Asetilkolin (Ach) & norepinefrin (NE)

• Neuron kolinergik spesifik

▫ Antagonis kolinergik ↓ (atropin & skopolamin)

penurunan fungsi kognitif

▫ Agonis kolinergik ↓ (physostigmine & arecoline)

peningkatan fungsi kognitif

• Defisit kolinergik spesifik konsentrasi kolin

asetiltransferase ↓ Ach ↓

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Neurotransmitters

• NE ↓ disebabkan oleh defisit neuron di lokus

ceruleus.

• Dua neurotransmitter lain : neuroactive peptides

somatostatin dan corticotropin.

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Daftar pustaka• Kaplan & Sadock’s synopsis of psychiatry • Harrison’s principles of internal medicine,

17th ed• http://repository.usu.ac.id/bitstream/123456

789/29941/4/Chapter%20II.pdf• http://www.cnsspectrums.com/aspx/articled

etail.aspx?articleid=972• http://www.google.co.id/imgres?q=senile+p

laques&um=1&hl=id&sa=N&biw=1280&bih=737&tbm=isch&tbnid=uxPce4h9zKQisM:&imgrefurl=https://sharepoint.cisat.jmu.edu/isat/klevicca/Web/ISAT454/AB.HTM&docid=7jcQQKq0RwUSxM&imgurl=https://sharepoint.cisat.jmu.edu/isat/klevicca/Web/ISAT454/plak.gif&w=219&h=216&ei=x1UIUJ7vG4fJrAfp9dXBAg&zoom=1&iact=hc&vpx=371&vpy=158&dur=780&hovh=172&hovw=175&tx=75&ty=110&sig=113429218722492950823&page=1&tbnh=130&tbnw=132&start=0&ndsp=24&ved=1t:429,r:1,s:0,i:71

• http://www.nealhendrickson.com/mcdougall/2004nl/040600pualzheimer.htm

• http://journals.prous.com/journals/servlet/xmlxsl/pk_journals.xml_summary_pr?p_JournalId=2&p_RefId=1192677&p_IsPs=N

• http://www.melisa.vt.vc/tag/patofisiologi-demensia