Neuronal death and familial Alzheimer’s disease genes

نویسندگان
چکیده

برای دانلود باید عضویت طلایی داشته باشید

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

منابع مشابه

A rescue factor abolishing neuronal cell death by a wide spectrum of familial Alzheimer's disease genes and Abeta.

Through functional expression screening, we identified a gene, designated Humanin (HN) cDNA, which encodes a short polypeptide and abolishes death of neuronal cells caused by multiple different types of familial Alzheimer's disease genes and by Abeta amyloid, without effect on death by Q79 or superoxide dismutase-1 mutants. Transfected HN cDNA was transcribed to the corresponding polypeptide an...

متن کامل

Molecular and Cellular Mechanisms of Neuronal Plasticity in Normal Aging and Alzheimers Disease

Many people are trying to be smarter every day. How's about you? There are many ways to evoke this case you can find knowledge and lesson everywhere you want. However, it will involve you to get what call as the preferred thing. When you need this kind of sources, the following book can be a great choice. molecular and cellular mechanisms of neuronal plasticity in normal aging and alzheimers di...

متن کامل

Magnesium and Alzheimers Disease: The Cholinergic Hypothesis

The cholinergic deficit in Alzheimer’s disease (AD) remains the cornerstone for the understanding of chemical signal transfer. Hypofunctions of cholinergic systems are significantly involved in the signs and symptoms of senile dementia of the Alzheimer type. Cognitive deficits in AD have been widely associated with dysfunction of the cholinergic system. As a diagnostic marker of AD the activity...

متن کامل

P3: Neuronal Death Following Posttraumatic Excitability and Seizure

لطفاً به چکیده انگلیسی مراجعه شود.

متن کامل

ذخیره در منابع من


  با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید

ژورنال

عنوان ژورنال: Japanese Journal of Pharmacology

سال: 2000

ISSN: 0021-5198

DOI: 10.1016/s0021-5198(19)47501-x