Studiu: Apariţia maladiei Alzheimer poate fi împiedicată prin mutaţia unei gene

3 Comentarii [+] Adauga un comentariu

#1 Cornelia Vodoiu 13.01.2010 23:01

• Raspunde

A.[« Longevity Gene » Helps Prevent Memory Decline And Dementia.
Article Date : 13 Jan. 2010 -5 :00 PST.
SOURCE : Deidre Branley ; Albert Einstein College of Medicine.
Scientists at Albert Einstein College of Medicine of Yeshiva University have found that a « longevity gene » helps to slow age- related decline in brain function in older adults. Drugs that mimic the gene ‘s effect are now under development , the researchers note, and could help protect against Alzheimer’s disease.
The paper describing the Einstein study is published in the January 13 edition of the Journal of the American Medical Association.
« Most work on the genetics of Alzheimer’s disease has focused on factors that increase the danger », said Richard B Lipton, M.D. the Lotti and Bernard Benson Faculty Scholar in Alzheimer’s Disease and professor and vice chair in the Saul R. Korey Department of Neurology at Einstein and senior author of the paper. As an example, he cites APOEε4, a gene variant involved in cholesterol metabolism that is known to increase the risk of Alzheimer’s among those who carry it.
In a 2003 study, Dr.Lipton and his colleagues identified the CHOLESTEROL ESTER TRANSFER PROTEIN (CETP) gene variant as a « longevity gene » in a population of Ashkenazi Jews.
The favorable CETP gene variant increases blod levels of high-density lipoprotein (HDL) –the so-called good cholesterol-and also results in larger –than – average HDL and low-density lipoprotein (LDL) particles.
The researchers of the current study hypothesized that the CETP longevity gene might also be associated with less cognitive decline as people grow older. To find out , they examined data from 523 participants from the Einstein Aging Study, an ongoing federally funded project that has followed a racially and ethnically diverse population of elderly Bronx residents for 25 years. »] SOURCE : Medical News TODAY.
B. Exista si un punct de vedere romanesc:
« Boala Alzheimer este caracterizata morfopatologic printr-o atrofie cerebrala moderata, dar difuza, cu debut obisnuit si predominant in regiunea parieto-occipitala si respectarea constanta a circumvolutiilor centrale.Boala constituie cea mai frecventa atrofie corticala a perioadei presenile, atingand un nivel maxim intre 50 si 60 de ani si o medie de 53 de ani (cunoscandu-se insa si forme precoce inainte de 40 de ani sau, exceptional de rar, forme juvenile), si predomina net la * feminin. Nu s-a putut incrimina un determinism genetic , dar nu poate fi exclusa o oarecare predispozitie familiala , pe fondul careia actioneaza multiplii factori favorizanti (traumatisme cranio-cerebrale , hipoxie-anoxie cerebrala, intoxicatii, tulburari metabolice generale cu rasunet cerebral etc.), boala fiind considerata – desi discutabil – ca o eredodegenerescenta.Tabloul clinic al bolii Alzeimer , expilicat prin bilateralitatea leziunilor cu predominanta cerebrala posterioara , este dominat in faza de debut (ce se esaloneaza de-a lungul a 2-4 ani) de tulburari de memorie (deficit mnezic global si progresiv ), tulburari de orientare spatiala intense si precoce, carora li se adauga unele tulburari ale functiilor simbolice (apraxie, alexie, agrafie si mai rar afazie) si o stare de apatie. Faza de stare este dominata de starea dementiala masiva , care intereseaza toate functiile intelectuale , printre care atentia (lipsa de concentrare), memoria (atat cea de inregistrare recenta, cat si cea evocatoare), orientarea (dezorientare temporo-spatiala), judecata, inteligenta etc. ; se mai adauga un sindrom afazic (afazia Wernicke, parafazia, jargonofazia, logoreea, palilalia, ecolalia etc.), un sindom apraxic (apraxia ideatorie, ideo-motorie, de imbracare, constructiva, apraxia pentru desen etc.), un sindrom agnozic (tulburari gnozice vizuale , ca agnozia vizuala, prosopagnozia etc., care nu se asociaza cu hemianopsie), tulburari psihice (idei delirante, de persecutie, deliruri onirice, de gelozie etc.) si tulburari de comportament (incetineala si apatie, uneori intrerupata de accese de agitatie incoerenta, un umor cu nuante depresive etc.). In ultima vreme in etiologia bolii Alzheimer , in afara de un determinism genetic, s-a incriminat si actiunea unui virus cu actiune lenta , care ar actiona asupra creierului, sau A UNEI CONCENTRATII CRESCUTE DE ALUMINIU IN MEDIUL INCONJURATOR. » Gh.Badiu, I.Teodorescu Exarcu – « Fiziologia si fiziopatologia sistemului nervos » , Ed.Medicala Bucuresti 1978, p.65.
Multa sanatate !

 

#2 Om 14.01.2010 01:12

• Raspunde

Salut

 

#3 EBA 14.01.2010 08:39

• Raspunde

EUS UNT MAI PROASTA SI NU INTELEG... SI DACA AM GENE FALSE, POT SA MI LE MUT SI EU, NU-I ASA?

 

Vezi toate »