March 20, 2018

Health Roundup - Alzheimer's Edition and breakthrough for Dementia with Lewy bodies (DLB) and the surprising effect of an Alzheimer's drug

Revolutionary Treatment? Scientists Successfully Reverse Alzheimer’s Disease In Mice

A major breakthrough in the war against Alzheimer’s disease may pave the way for one of the most effective treatments to date. A team of scientists say they have successfully reversed the disease in mice. Many more trials, tests, and hours of research remain before their method can be tried on humans, but it’s an historic step in the right direction. The researchers, based at the Cleveland Clinic Lerner Research Institute, found that by gradually reducing an enzyme in the brain called BACE1, they reversed the formation of amyloid plaques in the brains of mice with Alzheimer’s disease, improving their cognitive function. The scientists hope that this research will eventually produce drugs aimed at this enzyme in human brains.

“To our knowledge, this is the first observation of such a dramatic reversal of amyloid deposition in any study of Alzheimer’s disease mouse models,” says researcher Riqiang Yan in a news release by the Rockefeller University press.

More Alzheimer's Has Been Reversed in Mice With This Single Enzyme Treatment

Researchers were able to reverse the formation of amyloid plaques, which gradually kill neurons in patients with Alzheimer's disease, in the brains of mice - essentially reversing the condition.  Alongside the reduction of plaques that impair communication between brain cells, the mice also experienced cognitive improvement. The team from the Cleveland Clinic Lerner Research Institute in the US detailed the findings in the Journal of Experimental Medicine.

The authors achieved the promising set of results by gradually depleting an enzyme that plays a part in the formation of the plaques, known as BACE1.  One of the most concrete ways in which Alzheimer's is identified in a patient is through an abnormal buildup of beta-amyloid peptide, a protein that can build into the large amyloid plaques in the brain that are a telltale sign of the deadly, and to date incurable disease.  BACE1 helps to produce beta-amyloid peptide, and so inhibiting the enzyme with drugs could ultimately open the door to effective Alzheimer's treatments by halting the buildup.

 Bace1 Effect On Mice
Left: A mouse with Alzheimer's disease shows red amyloid plaques and green activated microglial cells.
Right: The brain that has gradually lost BACE1. (Hu et al., 2018)

Still more Scientists Make Major Breakthrough In Fight Against Alzheimer’s Disease

Scientists at the the Cleveland Clinic Lerner Research Institute have successfully reversed Alzheimer's disease in mice, a major breakthrough researchers are hopeful will translate into treatment for humans in the near future. The study was first published in the Journal of Experimental Medicine on February 14.Researchers found that the deletion of BACE1 in adult mice reversed amyloid deposition and improved cognitive functions.

"One of the earliest events in Alzheimer’s disease is an abnormal buildup of beta-amyloid peptide, which can form large, amyloid plaques in the brain and disrupt the function of neuronal synapses. Also known as beta-secretase, BACE1 helps produce beta-amyloid peptide by cleaving amyloid precursor protein (APP)," explains the Rockefeller University Press release.

The scientists successfully "generated mice that gradually lose this enzyme as they grow older. These mice developed normally and appeared to remain perfectly healthy over time," notes the release.
“Our study provides genetic evidence that preformed amyloid deposition can be completely reversed after sequential and increased deletion of BACE1 in the adult,” said Yan. “Our data show that BACE1 inhibitors have the potential to treat Alzheimer’s disease patients without unwanted toxicity. Future studies should develop strategies to minimize the synaptic impairments arising from significant inhibition of BACE1 to achieve maximal and optimal benefits for Alzheimer’s patients.”

As noted by Study Finds, there are still many more trials and test that must be completed before there can be testing on humans, but this latest discovery is "an historic step in the right direction."

Breakthrough for Dementia with Lewy bodies (DLB), the type Robin Williams suffered before committing suicide. 

Studies have determined the causes of dementia with Lewy bodies (DLB), he third most common form of dementia after Alzheimer's and vascular dementias. The discovery was made with extremely powerful scanning devices used in DLB for the first time.  The drugs could stop it 'in its tracks' by targeting a key chemical called alpha-synuclein, according to researchers.  The rogue protein is one of four types believed to be behind the devastating neurological disorder.  It disrupts brain cells in dementia with Lewy bodies - also known as DLB that is progressive and gets worse over time. Brain tissue from people who died from it showed the protein builds up in vital parts of neurons that connect cells. These may jump from one cell to another through these connections, say the international team led by Edinburgh University.

The findings shed light on the causes of DLB and will help to speed up the search for a treatment, they say.
Symptoms include problems with memory and judgment, feeling faint and developing tremors.  'These discoveries should invigorate the search for therapies aimed at reducing synaptic damage and open the possibility of targeting the spread of alpha-synuclein through the brain - which could stop disease progression in its tracks.'

An Alzheimer's Drug Has Been Shown to Help Teeth Repair Cavities Naturally  No fillings, no drills.

Dental fillings may soon be left in the ash heap of history, thanks to a recent discovery about a drug called Tideglusib.
Developed for and trialled to treat Alzheimer's disease, last year scientists found the drug also happens to promote the natural tooth regrowth mechanism in mice, allowing the tooth to repair cavities.

Tideglusib works by stimulating stem cells in the pulp of teeth, the source of new dentine. Dentine is the mineralized substance beneath tooth enamel that gets eaten away by tooth decay. Teeth can naturally regenerate dentine without assistance, but only under certain circumstances. The pulp must be exposed through infection (such as decay) or trauma to prompt the manufacture of dentine.
But even then, the tooth can only regrow a very thin layer naturally - not enough to repair cavities caused by decay, which are generally deep. Tideglusib changes this outcome because it turns off the GSK-3 enzyme, which stops dentine from forming.

In the 2017 research, the team inserted small, biodegradable sponges made of collagen soaked in Tideglusib into cavities. The sponges triggered dentine growth and within six weeks, the damage was repaired. The collagen structure of the sponges melted away, leaving only the intact tooth. Thus far, the procedure has only been used in mouse teeth.
Posted by Jill Fallon at March 20, 2018 12:38 PM | Permalink