Loss of Volume in the Cerebellum Correlates with Memory Decline with Age

The brain is known to shrink with age, by about 5% per decade in later adult life, though the underlying processes leading to this loss of volume are not well understood in detail. The research here adds to existing evidence for loss of volume to correlate with loss of cognitive function. It is unclear as to what can be done specifically to address this issue beyond developing the means to repair the list of damage and dysfunction that causes aging, and observing the results as repair therapies are deployed, first in animals, and then in humans.

The human cerebellum plays an essential role in motor control, is involved in cognitive function and helps to regulate emotional responses. However, little is known about the relationship between cerebellar lobules and age-related memory decline. We aimed to investigate volume alterations in cerebellar lobules at different ages and assess their correlations with reduced memory recall abilities.

A sample of 275 individuals were divided into the following four groups: 20-35 years (young), 36-50 years (early-middle age), 51-65 years (late-middle age), and 66-89 years (old). Volumes of the cerebellar lobules were obtained using volBrain software. Group differences in cerebellar lobular volumes were assessed, and multiple comparisons were used to investigate the relationship between lobular volumes and memory recall scores.

We found that older adults had smaller cerebellar volumes than the other subjects. Volumetric decreases in size were noted in bilateral lobule VI and lobule crus I. Moreover, the volumes of bilateral lobule crus I, lobule VI, and right lobule IV were significantly associated with memory recall scores. Thus some lobules of the cerebellum appear more predisposed to age-related changes than other lobules. These findings provide further evidence that specific regions of the cerebellum could be used to assess the risk of memory decline across the adult lifespan.

Link: https://doi.org/10.21037/qims.2019.10.19


Isn't there a study showing a prevention of volume loss with daily fish oil intake?

Posted by: Nathan McKaskle at January 31st, 2020 12:07 PM

Hi Nathan! Just a2 cents.

Yes, many of them, studies said that omega-3 intake, of long-chain nature (DHA/EPA and to a certain degree LNA (linolenic acid 18:3 (LNA), rather than linoleic acid 18:2 (LA, Omega-6) elevates total brain long chain O-3 PUFAs (again there is production and incorporation of DHA/EPA in mitochondrial membranes' phospholipids (mainly, phosphatidylcholine/phosphaditylethanolamine, of neurons). Omega-3 DHA, and to a lesser extent, EPA, activate epigenetic signals to reduce inflammation and improve mitochondrial membrane kinetics (it's not so much the lipids, it'S the kinetics of it that make the membrane more fluid/fluidized and as such, faster - faster correction of problems (if rigid 'solid/waxy' state). They say a correlatoin between total intake of long-chain O3 (DHA/EPA) or short-chain O3 (LNA), or all three; The downshoot is 'aging', omega-3 are 'healthy aging' promoters. They age you, just 'nicely'/healthily. Because, you get function from them, but, alas, they are a Double-Edge Sword. They reorder membrane function but, are Very susceptible (at least the long chain ones by number of kinks/double-bonds), they have many 'Attack points' for ROS to Attack on. While LNA is better because it is short-chain O3; and, they saw that LNA ended up beneficial because it would increase total DHA/EPA levels (by desaturate and elongase Activity that would 'Elongate/Desaturate' LNA to Long Unsaturated Version (PolyUnsaturates Fatty Acids/PUFAs) to DHA/EPA, being the longest and most susceptible ones (they 320X more peroxidizable than Mono-unsaturates (such Oleic Acid 18:1, 1 kink, not much to Attack thus unsusceptible to 'Lipid Peroxidation problem/Peroxidizability''. Called PI (Peroxidizability Index). Our brains are Very High in PI, but, our O3s allow us 'fast thinking/neuron function' (otherwise we would be vegetative or dead), yet, they kills us because are susceptible. ANimals have a Reduction of Longchian PUFAs with longevity. Because evolution found a way to reorder PUFA/mitolipidome towards Less Unsaturation and More Saturation (Unsusceptible to ROS Attack in mitos at Complex I). Thankfully, most studies showed an Exception to this rule/or general observation in most animals organs - except, the brain. The brain can have High PI and the animal will Stil live Very Long life, because the brain has more Compensatory ROS Consumption to conpensate, so that O3 negative effect is Nullified. And yes, as you said, o3 levels were correlated with grey and white matter loss; especially in late senior age (senile had more brain matter loss (white/gray) and showed PUFA delipidation/more destruciton of their PUFAs due to brain diseases (Alzheimers/Parkinson/dementia/brain degenerescence cause mitochondrial destruction peroxidation of their PUFAs (and then their loss, so you could see a Lower PI in their brains..yet they still aged faster; because of brain matter attrition/skrinking/pruning; same thing as thymic involution/thymus pruning). It is why they suggest children of mothers with less O3 may have (had) O3 lackings in brain, and the children may suffer brain deficience (this early in life). Safe to say, if you can think Fast/Sharp..you probabl have High levels of O3 and improve your chance of living to a 100 (because famous chess players or mathematicians (Genius people) lived to be centenarians - because they kept their brain/O3, kept thinking and not become demented/Alzheimer/lose brain matter as they age).
Long story, short, continue taking O3/fish oïl/eat fish if doing so (just be careful of dose and peroxidized cheap products which will cause you More damage then good; because you Must Quench the ROS/peroxidation from using longchain O3 (2-faced/double-edged)).

Just a 2 cents.

Posted by: CANanonymity at January 31st, 2020 5:59 PM
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