Unraveling the Thriller Behind Alzheimer’s Resilience

By Kerry Blackadar

If you happen to have been to shrink right down to the dimensions of a single cell and peer contained in the mind of an individual with Alzheimer’s illness, you’d discover a labyrinth of protein clumps and sticky, thread-like constructions.

Often called amyloid plaques and neurofibrillary (or tau) tangles, these irregular accumulations of protein fragments within the mind are the hallmarks of Alzheimer’s illness. Over time, they intrude with the mind’s capacity to perform by hampering communication between neurons, in the end triggering the telltale indicators of the illness, like reminiscence loss.

Mysteriously, the brains of some seemingly wholesome older people — these with no indicators of dementia — will also be riddled with plaques and tangles. These people, for all intents and functions, are “resilient” to Alzheimer’s.

Right this moment, UBC scientists are on a daring mission to know this resilience at a deeper stage, with the hope that what they uncover might maintain the important thing to revolutionizing therapy for the devastating illness.

“If we can get to the bottom of why a person with no symptoms of cognitive decline has the same brain pathology as someone with Alzheimer’s, then we could look to mimic or harness that resiliency and find new therapeutics,” says UBC’s Dr. Haakon Nygaard, the Fipke Professor in Alzheimer’s Analysis and director of the UBC Hospital Clinic for Alzheimer Illness and Associated Issues.

To assist unravel the thriller behind Alzheimer’s resilience, Nygaard is collaborating with UBC scientists who’re embracing a number of the world’s newest advances in stem cell know-how, 3D bioprinting, next-generation neuroimaging, and single-cell transcriptomics.

Their journey begins with rising “mini-brains” in a petri dish.

From blood cells to 3D “mini-brains”

Contained in the Djavad Mowafaghian Centre for Mind Well being at UBC, Nygaard fastidiously adjusts one of many settings on a 3D bioprinter — considered one of only some printers of its variety on the planet getting used to advance Alzheimer’s analysis.

A low hum fills the room as a robotic arm strikes into place and begins printing layers of mind cells right into a petri dish.

“Brain cells respond very differently in a 3D versus 2D environment,” says Nygaard. “With 3D bioprinting, and our other advanced 3D models, we’re essentially trying to replicate how brain cells actually function and interact with one another in the human body.”

Much like 3D printing, whereby a digital design is constructed layer upon layer, with a 3D bioprinter, a duplicate of dwelling human tissues is printed in skinny layers utilizing biomaterial.

Within the case of Nygaard’s lab, stems cells, derived from the blood of Alzheimer’s sufferers, are first reprogrammed into mind cells. Then, utilizing the bioprinter or different tissue engineering strategies, three-dimensional tissue fashions resembling areas of the affected person’s mind are generated, together with microscopic, ball-like constructions referred to as “neurospheres.”

“These 3D human brain cell models are allowing us to gain greater insights into the basic cellular mechanisms that cause the brain to degenerate in Alzheimer’s,” says Nygaard.

Already, as a part of a pioneering analysis mission with UBC’s Dr. Brian MacVicar, professor of psychiatry and Canada Analysis Chair in Neuroscience, the 3D neurosphere mannequin has been used to look at the position that oxidative stress (the imbalance of free radicals and antioxidants) performs within the demise of mind cells of Alzheimer’s sufferers.

Utilizing state-of-the-art neuroimaging methods, MacVicar, a world chief in neuroinflammation, and his crew are in a position to provide an unparalleled visualization of the mobile processes happening in infinitesimal areas, some solely 100 micrometres (one millionth of a metre) broad.

To this point, utilizing the 3D mannequin, they’ve proven that microglia — the immune cells of the mind — provide safety from the injury brought on by oxidative stress triggered by the presence of amyloid.

“Here we can see how the neurons interact with the microglia,” says MacVicar, pointing to a rotating fluorescent picture of a neurosphere. “By studying these individual interactions between the cell types, we can shed new light on how Alzheimer’s starts.”

And, because of an in depth collaboration with UBC’s Dr. Freda Miller, professor within the Division of Medical Genetics and a number one stem-cell knowledgeable, the analysis crew has been in a position to achieve even larger insights — isolating single cells to look at genetic components at play.

“By looking at gene expression profiles in the individual brain cells, we’re on the path to addressing questions in Alzheimer’s research that would not have been possible only a short time ago,” says Miller.

That features addressing the query of Alzheimer’s resiliency.

In keeping with Miller, who brings a novel perspective to the analysis collaboration as a developmental neurobiologist learning how stem cells construct the mind, resiliency is a very necessary analysis frontier in Alzheimer’s.

“Traditionally, the world has asked: Why do people get dementia? But we’re flipping that on its head and asking an equally important question: Why do some people not get dementia?”

May resiliency be the lacking hyperlink to understanding Alzheimer’s?

Whereas nobody is aware of precisely how many individuals are literally “resilient” to Alzheimer’s illness, Nygaard estimates about 20-30 per cent of older adults have related ranges of amyloid of their brains to that of somebody with Alzheimer’s, but exhibit no indicators of dementia.

“By studying those who have escaped or delayed developing dementia, our hope is to understand what’s driving that protection,” says Nygaard.

Within the coming years, the crew will construct on their newest work, producing 3D “mini-brains” of individuals with Alzheimer’s resiliency — making use of the identical highly effective neuroimaging and genetic evaluation methods.

“Once we understand the cellular and genetic mechanisms at the root of resiliency, the hope is to harness that resilience to guide the discovery of new treatments or even repurpose existing drugs that could one day stop — or even reverse — progression of Alzheimer’s disease,” says MacVicar.

In keeping with Nygaard, the time to seek out new remedies for Alzheimer’s sufferers is now.

“As a physician, if your patient gets a bacterial infection, you can give them antibiotics. If your patient breaks their leg, you can fix it. But if your patient is diagnosed with Alzheimer’s, there’s still relatively little we can offer them. There is no cure,” says Nygaard, who works straight with Alzheimer’s sufferers and households as a neurologist.

Through the years, Nygaard has watched his sufferers being slowly robbed of their identities, reminiscence by reminiscence. And he’s watched households robbed of their family members, sooner or later at a time.

“We still don’t have a treatment that can stop the progression of Alzheimer’s, and that really haunts me,” says Nygaard. “But it also keeps me motivated.”

On the finish of the day, it’s the numerous sufferers and their households who’re the driving power behind Nygaard’s analysis — as properly of these of his collaborators.

“Imagine if we could give even 10 more good years to people who are in the early stages of Alzheimer’s,” says Miller, who strongly believes the teachings they study Alzheimer’s resiliency might sooner or later be utilized to different neurodegenerative illnesses, together with Parkinson’s.

“The potential of this research is enormous.”

—

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