Why do the brains of alzheimer's patients shrink in new ways?

The number of people with alzheimer's disease is increasing year by year, with more than 10 percent of patients aged 65 and older.

Alzheimer's disease (AD) is a chronic neurological decline associated with aging, with typical symptoms including memory loss, cognitive impairment, and language decline.

It threatens the health and life of the world's more than 44 million elderly people.

Existing treatment drugs can only alleviate the symptoms of alzheimer's disease, can't repair the damage caused by the brain, and cannot effectively prevent and control the deterioration of the disease.

In 1901, Dr. Alois Alzheimer, a neuropathologist in Germany, met a woman with Alzheimer's who had severe memory problems, a lack of direction, and occasional gibberish.

In 1906, the patient died, and Dr. Alzheimer performed an autopsy on her, finding that her brain tissue shrank, her weight was reduced, her brain cortices and the hippocampus shrank.

At the same time, neurons in the cortex die in large Numbers, and there are precipitations of special substances.

Alois Alzheimer (German) the doctor

In 1907, Dr. Alzheimer published a lengthy paper describing his discovery until 1910, when dementia with these manifestations was finally named "Alzheimer's disease" (AD).

To find out, we need to dig deep into the pathogenesis of alzheimer's disease and find the molecular mechanism of the decay of brain cells.

A recent academic paper published online in Nature Neuroscience reveals new pathways for brain cell death in AD patients.

From Arizona state university - Banner Health neuroscientist Salvatore Oddo and from the Translational Genomics research institute (TGen), the team at the university of California for the first time confirmed necroptosis (necrotizing apoptosis) can lead to neuronal cell death, resulting in deterioration of alzheimer's disease, brain atrophy and cognitive decline.

Necroptosis is the process by which a series of proteins trigger cells from the inside out.

Studies have shown that necroptosis is associated with multiple sclerosis, amyotrophic lateral sclerosis (ALS).

Now, for the first time, scientists have confirmed that it is also involved in alzheimer's disease.

Necroptosis was initially caused by inflammation.

Three key proteins - RIPK1, RIPK3 and MLKL - contributed to the onset of necrotic apoptosis.

Past studies have shown that RIPK1 and RIPK3 proteins form a filamentous complex called "necrosome".

Now, the Oddo team has found that necrosis can be activated by necrosis.

It activates the MLKL protein, which further affects the mitochondria of the cell and eventually leads to cell death.

"MLKL plays a key role in the process of cell necrosis," said professor Winnie Liang, associate professor at TGen.

Subsequently, they found a signaling pathway associated with cell necrosis: RIPK1 was combined with RIPK3 to form a complex that further activated the MLKL protein.

How can you slow down these vicious cycles?

The team confirmed by using AD mice that blocking the RIPK1 could inhibit the necroptosis pathway, thereby slowing the death of nerve cells.

More importantly, the mice that had been inhibited by the necroptosis pathway showed better cognitive abilities.

The study will provide new hope for alzheimer's research and targeted therapy.

prev:How to make a combo diagram?(2017-08-07)

next:These three software can handle PCR primers design(2017-08-08)