Category: Dementia

The drug healed synaptic connections in the brain and memories were partially restored.

A new drinkable cocktail of drugs provides hope for stopping the progression of Alzheimer’s.

An old antibiotic — called Suprax — has been shown to reverse the memory problems linked to Alzheimer’s.

Now that the study on mice has been successful, the team hope to go on and test it on Alzheimer’s patients.

There are currently no drugs that effectively treat Alzheimer’s, only therapies that may help slow cognitive decline and reduce symptoms.

The team — based at Yale University — have been searching for compounds that will interfere with the first stages of the disease.

Professor Stephen Strittmatter, study co-author, said:

“We wanted to find molecules that might have a therapeutic effect on this network.”

After screening thousands of different compounds, they came across an old antibiotic, known as Suprax.

This seemed to have the desired effect of stopping Alzheimer’s in its tracks.

The tests on mice showed that the compound healed synaptic connections in the brain and their memories were partially restored.

The next step is to check that the compound is not toxic before human trials can begin.

The study was published in the journal Cell Reports (Gunther et al., 2019).

The common drink contains compounds called phenylindanes that may help protect against dementia.

Drinking coffee could protect against both Alzheimer’s and Parkinson’s, new research suggests.

The study looked at compounds in coffee called phenylindanes, which may help protect against dementia.

Higher levels of phenylindanes typically make coffee taste more bitter.

Dr Donald Weaver, study co-author, said:

“Coffee consumption does seem to have some correlation to a decreased risk of developing Alzheimer’s disease and Parkinson’s disease.

But we wanted to investigate why that is — which compounds are involved and how they may impact age-related cognitive decline.”

The study examined how phenylindanes interact with two proteins that are critical to the development of Alzheimer’s and Parkinson’s.

The results showed that phenylindanes inhibit both beta amyloid and tau proteins.

The researchers also compared dark roast, light roast and decaffeinated coffees.

It found that dark roasts had the highest quantities of phenylindanes.

Caffeine, though, made no difference, explained Dr Ross Mancini, the study’s first author:

“The caffeinated and de-caffeinated dark roast both had identical potencies in our initial experimental tests.

So we observed early on that its protective effect could not be due to caffeine.”

Dr Weaver said it is a major advantage that coffee is a natural crop:

“Mother Nature is a much better chemist than we are and Mother Nature is able to make these compounds.

If you have a complicated compound, it’s nicer to grow it in a crop, harvest the crop, grind the crop out and extract it than try to make it.”

More work will be required before therapies can be developed, Dr Weaver said:

“What this study does is take the epidemiological evidence and try to refine it and to demonstrate that there are indeed components within coffee that are beneficial to warding off cognitive decline.

It’s interesting but are we suggesting that coffee is a cure?

Absolutely not.”

The study was published in the journal Frontiers in Neuroscience (Mancini et al., 2018).

Italian researchers discover early sign of dementia related to high blood pressure.

Only somewhat elevated blood pressure in mid-life increases the risk of developing dementia by 45%, new research concludes.

Fifty-year-olds with blood pressure of more than 130/80 had the increased risk, a new study of over 9,000 people in the UK has found.

This level is only somewhat elevated (120/80mmHg is the top of the ideal range) and below the level at which hypertension is normally treated with drugs.

The damage from elevated blood pressure seems to accumulate over time, said study author Professor Archana Singh-Manoux:

“Our analysis suggests that the importance of mid-life hypertension on brain health is due to the duration of exposure.

So we see an increased risk for people with raised blood pressure at age 50, but not 60 or 70, because those with hypertension at age 50 are likely to be ‘exposed’ to this risk for longer.”

Detecting dementia early

In related findings, Italian researchers have been able to detect the earliest signals of neurological damage related to high blood pressure using a more powerful brain scanner.

It is hoped the finding will allow scientists to spot the damage when there is still a chance to treat it.

Dementia begins to damage the brain long before any symptoms emerge — at this point it is usually too late to treat it.

Professor Giuseppe Lembo, study author, said:

“The problem is that neurological alterations related to hypertension are usually diagnosed only when the cognitive deficit becomes evident, or when traditional magnetic resonance shows clear signs of brain damage.

In both cases, it is often too late to stop the pathological process”

The results come from hypertension patients given brain scans with a powerful 3-tesla MRI machine.

They found that people with high blood pressure had damage to critical parts of their brains.

They also scored lower on standard cognitive tests of processing, memory, learning and executive function.

Mr Lorenzo Carnevale, the study’s first author, said:

“We have been able to see that, in the hypertensive subjects, there was a deterioration of white matter fibers connecting brain areas typically involved in attention, emotions and memory,

An important aspect to consider is that all the patients studied did not show clinical signs of dementia and, in conventional neuroimaging, they showed no signs of cerebral damage.

Of course, further studies will be necessary, but we think that the use of tractography will lead to the early identification of people at risk of dementia, allowing timely therapeutic interventions.”

The studies were published in the European Heart Journal and the journal Cardiovascular Research (Abell et al., 2018; Carnevale et al., 2018).