- The researchers autopsied 24 brains, including six from people known as “SuperAgers.”
- They found that SuperAgers had larger neurons than people almost 60 years younger.
- They noted that more research is needed to understand how larger neurons are related to preserved memory capacity in SuperAgers.
Memory capacity typically decreases with age. Around
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Further study of how SuperAgers maintain their memory capacity could help researchers develop preventive strategies and treatments for cognitive decline.
Researchers recently autopsied the brains of 24 people, including six dubbed “cognitive SuperAgers.”
They found that the neurons of SuperAgers were larger than those of those 20-30 years younger and that their neurons were not
“For reasons that are still unknown, cell populations in the [brain’s] entorhinal cortex (ERC) are selectively susceptible to tau tangle formation during normal aging and early stages of Alzheimer’s disease,” Dr. Tamar Gefen, an assistant professor of psychiatry and behavioral sciences at Northwestern University Feinberg School of Medicine in Chicago, and one of the study’s authors, says Medical news today.
“In this study, we show that neuronal shrinkage (atrophy) in the ERC appears to be a characteristic marker of [Alzheimer’s disease]. We hypothesize that this process is a function of tau tangle formation in the affected cells, [and that it leads] poor memory performance in old age. Identifying this contributing factor is critical for early detection of Alzheimer’s, monitoring its progression and guiding treatment,” she explained.
The study appears in Journal of Neuroscience.
For the study, researchers autopsied the brains of:
- six SuperAgers with an average age of 91 years
- seven “cognitively average” older people with a mean age of 89 years
- six healthy younger adults between the ages of 26 and 61
- five adults with mild cognitive impairment (MCI) with a mean age of 92 years.
At the time of death, all participants were able to engage in activities of daily living, and all were free of clinical signs or history of neurological or psychiatric disorders.
The researchers found no difference in years of schooling, brain weight, or postmortem interval between the groups.
They also tested ApoE Genotypes using DNA from patient blood samples. Among the participants, only one person from the MCI group had the
The researchers assessed a cross-sectional layer of neurons from layers II, III and V of the participants’ ERC. The ERC consists of six neuronal layers and is one of the first areas to develop signs of Alzheimer’s disease.
In particular, they assessed overall neuronal health and the presence of neurofibrillary tangles (NFT), also known as tau proteins, which when collected in neurons cause neuronal dysfunction.
In the end, the researchers found that Layer II ERC neurons were significantly larger in SuperAgers than other groups, including younger controls, some 60 years younger than them.
They further found that those in the “cognitively average” group of elderly had more than twice the NFT density of SuperAgers in layer II of the ERC.
When asked why SuperAgers’ neurons might be larger than those of their peers, Dr. James Giordano, Professor of Neurology and Biochemistry at Georgetown University Medical Center in Washington MNT:
“Possibly these are meganeurons that have a genetic predisposition and/or an environmental tendency to increase in size to allow for greater intra- and intercellular information processing. In this way, these neurons could have mechanisms that enhance both their functionality and their resilience or resilience to metabolic stress and degradation.”
“The increased size of these neurons may reflect a greater magnitude or variety of intracellular functions, including a larger network of cellular machinery that enable detoxification, reduced susceptibility to inflammation, and improved stability of metabolic activity in and across a variety of micro- and macro-environments enable conditions,” he added.
dr Gefen noted, “One possibility for the larger size is that these neurons are protected from neurofibrillary tangles – a hallmark of Alzheimer’s disease. We’re not yet sure why these neurons were larger in SuperAgers or why they are relatively protected from disease.”
The researchers wrote that this protection occurs despite other age-related brain changes in SuperAgers.
They also wrote that their results suggest that increased NFT levels lead to neuronal shrinkage. They found that this observation was particularly evident in the MCI group, which had significantly smaller cell size than other groups.
They further explained that larger layer II ERC neurons in SuperAgers than in their young peers could indicate that large ERC cells were present from birth and are structurally conserved throughout life.
“Future in-depth studies are needed to understand how and why neuronal integrity is preserved in SuperAgers. For example, I’m interested in studying the cellular environment – what chemical, metabolic or genetic properties of these cells make them resilient?’ added friends.
“We will also want to study other ‘hubs’ along the brain’s memory circuitry to better understand disease spread or resistance,” she noted.
The researchers concluded that SuperAgers carry a unique biological signature made up of larger, healthier ERC neurons that are relatively free of tau tangles.
When asked about the study’s limitations, Dr. Believed that their results were limited by their small sample size. She pointed out that her small sample size was partly because SuperAgers were “unique and rare.”
She continued, “Perhaps one of the most important messages is that, critical to understanding brain disease, is that we learn about human biology (both normal and abnormal) in life – and in death.” Our SuperAgers pledge to donate their autopsied brains for research. I have the fortunate opportunity to know my patients and research participants intimately, both living and dying.”
dr Giordano noted that the study has opened the door for further exploration of the function of these “unique neurons” – “both alone and in collaboration with other cells, nodes and networks of the brain and body”.
“Another important question [for future investigation] is why and how some people develop these oversized cells while others don’t. Taken together, such studies may provide improved insights into the cognitive functionality and relative resilience and/or resilience of SuperAgers to neurodegenerative diseases. This allows us to identify and design new interventions that could potentially preserve cognitive function throughout the lifespan,” he added.
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