hippocampus

means "sea horse", and is named for its shape. It is one of the oldest parts of the brain, and is buried deep inside, within the limbic lobe. The hippocampus is important for the forming, and perhaps long-term storage, of associative and episodic memories. Specifically, the hippocampus has been implicated in (among other things) the encoding of face-name associations, the retrieval of face-name associations, the encoding of events, the recall of personal memories in response to smells. It may also be involved in the processes by which memories are consolidated during sleep.

Gist memory may be why false memories are more common in older adults

  • Gist processing appears to play a strong role in false memories.
  • Older adults rely on gist memory more.
  • Older adults find it harder to recall specific sensory details that would help confirm whether a memory is true.

Do older adults forget as much as they think, or is it rather that they ‘misremember’?

A small study adds to evidence that gist memory plays an important role in false memories at any age, but older adults are more susceptible to misremembering because of their greater use of gist memory.

Gist memory is about remembering the broad story, not the details. We use schemas a lot. Schemas are concepts we build over time for events and experiences, in order to relieve the cognitive load. They allow us to respond and process faster. We build schemas for such things as going to the dentist, going to a restaurant, attending a lecture, and so on. Schemas are very useful, reminding us what to expect and what to do in situations we have experienced before. But they are also responsible for errors of perception and memory — we see and remember what we expect to see.

As we get older, we do of course build up more and firmer schemas, making it harder to really see with fresh eyes. Which means it’s harder for us to notice the details, and easier for us to misremember what we saw.

A small study involving 20 older adults (mean age 75) had participants look at 26 different pictures of common scenes (such as a farmyard, a bathroom) for about 10 seconds, and asked them to remember as much as they could about the scenes. Later, they were shown 300 pictures of objects that were either in the scene, related to the scene (but not actually in the scene), or not commonly associated to the scene, and were required to say whether or not the objects were in the picture. Brain activity was monitored during these tests. Performance was also compared with that produced in a previous identical study, involving 22 young adults (mean age 23).

As expected and as is typical, there was a higher hit rate for schematic items and a higher rate of false memories for schematically related lures (items that belong to the schema but didn’t appear in the picture). True memories activated the typical retrieval network (medial prefrontal cortex, hippocampus/parahippocampal gyrus, inferior parietal lobe, right middle temporal gyrus, and left fusiform gyrus).

Activity in some of these regions (frontal-parietal regions, left hippocampus, right MTG, and left fusiform) distinguished hits from false alarms, supporting the idea that it’s more demanding to retrieve true memories than illusory ones. This contrasts with younger adults who in this and previous research have displayed the opposite pattern. The finding is consistent, however, with the theory that older adults tend to engage frontal resources at an earlier level of difficulty.

Older adults also displayed greater activation in the medial prefrontal cortex for both schematic and non-schematic hits than young adults did.

While true memories activated the typical retrieval network, and there were different patterns of activity for schematic vs non-schematic hits, there was no distinctive pattern of activity for retrieving false memories. However, there was increased activity in the middle frontal gyrus, middle temporal gyrus, and hippocampus/parahippocampal gyrus as a function of the rate of false memories.

Imaging also revealed that, like younger adults, older adults also engage the ventromedial prefrontal cortex when retrieving schematic information, and that they do so to a greater extent. Activation patterns also support the role of the mediotemporal lobe (MTL), and the posterior hippocampus/parahippocampal gyrus in particular, in determining true memories from false. Note that schematic information is not part of this region’s concern, and there was no consistent difference in activation in this region for schematic vs non-schematic hits. But older adults showed this shift within the hippocampus, with much of the activity moving to a more posterior region.

Sensory details are also important for distinguishing between true and false memories, but, apart from activity in the left fusiform gyrus, older adults — unlike younger adults — did not show any differential activation in the occipital cortex. This finding is consistent with previous research, and supports the conclusion that older adults don’t experience the recapitulation of sensory details in the same way that younger adults do. This, of course, adds to the difficulty they have in distinguishing true and false memories.

Older adults also showed differential activation of the right MTG, involved in gist processing, for true memories. Again, this is not found in younger adults, and supports the idea that older adults depend more on schematic gist information to assess whether a memory is true.

However, in older adults, increased activation of both the MTL and the MTG is seen as rates of false alarms increase, indicating that both gist and episodic memory contribute to their false memories. This is also in line with previous research, suggesting that memories of specific events and details can (incorrectly) provide support for false memories that are consistent with such events.

Older adults, unlike young adults, failed to show differential activity in the retrieval network for targets and lures (items that fit in with the schema, but were not in fact present in the image).

What does all this mean? Here’s what’s important:

  • older adults tend to use schema information more when trying to remember
  • older adults find it harder to recall specific sensory details that would help confirm a memory’s veracity
  • at all ages, gist processing appears to play a strong role in false memories
  • memory of specific (true) details can be used to endorse related (but false) details.

What can you do about any of this? One approach would be to make an effort to recall specific sensory details of an event rather than relying on the easier generic event that comes to mind first. So, for example, if you’re asked to go to the store to pick up orange juice, tomatoes and muesli, you might end up with more familiar items — a sort of default position, as it were, because you can’t quite remember what you were asked. If you make an effort to remember the occasion of being told — where you were, how the other person looked, what time of day it was, other things you talked about, etc — you might be able to bring the actual items to mind. A lot of the time, we simply don’t make the effort, because we don’t think we can remember.

https://www.eurekalert.org/pub_releases/2018-03/ps-fdg032118.php

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Size of hippocampus associated with PTSD therapy benefits

  • Size of that key memory region, the hippocampus, appears to be not simply a risk factor for PTSD, but also key to whether sufferers will respond positively to exposure therapy.

Following previous research showing that having a smaller hippocampus is associated with increased risk of PTSD, a study involving 40 participants with PTSD and 36 trauma-exposed healthy controls has found that those PTSD patients who responded to the treatment had larger hippocampi compared to those who didn’t benefit from the therapy.

The participants were evaluated at baseline and after 10 weeks, during which time the PTSD group had prolonged exposure therapy.

The study found that both the resilient controls and the 23 patients with PTSD who responded to treatment had greater hippocampal volume at the beginning of the study than the 17 non-responders.

The findings add to growing evidence that the hippocampus is key to distinguishing between cues that signal safety and those that signal threat.

http://www.eurekalert.org/pub_releases/2016-05/cumc-sob051216.php

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Brain tissue structure could explain link between fitness and memory

  • Brain scans of healthy young adults found that higher aerobic fitness was associated with greater hippocampal elasticity, which was a better predictor of cognitive performance than hippocampal volume.

A new MRI technique has revealed that it is the structural integrity of the hippocampus more than its size that reflects fitness and correlates with cognitive performance.

Research has focused on hippocampal size because it is easier to measure, and in children and older adults there are strong correlations between hippocampal size and memory. But this is less true for healthy, young adults. This new, subtler, technique reveals that something else is going on — something that has probably been masked by the effects of size in older adults (whose hippocampi are shrinking) and younger children (whose brains are still growing).

The technique measures viscoelasticity. If the hippocampus is more elastic, memory is better. When it’s more viscous, memory is worse. Those with better aerobic fitness had better hippocampal elasticity.

https://www.eurekalert.org/pub_releases/2017-05/uoia-bts050117.php

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Inflamed iron-containing cells found in Alzheimer's brains

A post-mortem study of five Alzheimer's and five control brains has revealed the presence of iron-containing microglia in the subiculum of the Alzheimer's brains only. The subiculum lies within the hippocampus, a vital memory region affected early in Alzheimer's. None of the brains of those not diagnosed with Alzheimer's had the iron deposits or the microglia, in that brain region, while four of the five Alzheimer's brains contained the iron-containing microglia.

The microglia were mostly in an inflamed state. Growing evidence implicates brain inflammation in the development of Alzheimer's.

There was no consistent association between iron-laden microglia and amyloid plaques or tau in the same area.

Obviously, this is only a small study, and more research needs to be done to confirm the finding. However, this is consistent with previous findings of higher levels of iron in the hippocampi of Alzheimer's brain.

At the moment, we don't know how the iron gets into brain tissue, or why it accumulates in the subiculum. However, the researchers speculate that it may have something to do with micro-injury to small cerebral blood vessels.

This is an interesting finding that may lead to new treatment or prevention approaches if confirmed in further research.

http://www.eurekalert.org/pub_releases/2015-07/sumc-sss072015.php

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More evidence for a link between type 2 diabetes and Alzheimer’s

Glucose levels linked to cognitive decline in those with MCI

A study involving 264 older adults with mild cognitive impairment has found that those with normal glucose levels (167; 63%) had less cognitive decline over 2 years than those with impaired (high) glucose levels (97; 37%). They also showed less brain shrinkage and were less likely to develop Alzheimer’s. The fasting glucose levels were classified according to the American Diabetes criteria.

[3614] Vos SJB, Xiong C, Visser PJ, Jasielec MS, Hassenstab J, Grant EA, Cairns NJ, Morris JC, Holtzman DM, Fagan AM. Preclinical Alzheimer's disease and its outcome: a longitudinal cohort study. The Lancet Neurology [Internet]. 2013 ;12(10):957 - 965. Available from: http://www.thelancet.com/journals/laneur/article/PIIS1474-4422(13)70194-7/abstract

Rat study suggests cognitive decline in diabetics related to amyloid-beta buildup

A rat study supports the growing evidence of a link between type 2 diabetes and Alzheimer’s. In this study, 20 rats were fed a high-fat diet to give them type 2 diabetes. A subsequent test found that the diabetic rats had significantly poorer memories than the control group of rats on a healthy diet (the rats were taught to associate a dark cage with an electric shock; how long the rat continues to remember that the stimulus means a shock — as shown by their frozen reaction — is taken as a measure of how good their memory is; the diabetic rats froze for less than half the time of the controls).

The diabetic rats then had their brains (specifically, the hippocampus) injected with antibodies that disrupt amyloid-beta plaques. This produced no change in their behavior. However, when they were given antibodies that disrupt amyloid-beta oligomers (precursors of the plaques), the memory deficit was reversed, and they behaved the same as the healthy rats.

These findings suggest that the cognitive decline often seen in type 2 diabetes is not due to the disruption in insulin signaling, as thought, but rather the build-up of amyloid oligomers. Previous research has shown that the same enzymes break down both insulin and the oligomers, so when there’s a lot of insulin (which the enzymes prioritize), the enzymes don’t have as much opportunity to work on breaking down the oligomers. The oligomers collect, preventing the insulin from reaching their proper receptors in the hippocampus, which impairs cognitive function.

All this supports the idea that type 2 diabetes may be thought of as early-stage Alzheimer's. Obviously a lot more work needs to be done to confirm this picture, but certainly in the mean time, it can be taken as another reason to take type 2 diabetes very seriously.

www.newscientist.com/article/mg22029453.400-are-alzheimers-and-diabetes-the-same-disease.html

McNay, E.C., Osborne, D., et al. 2014. Preliminary data presented at the Society for Neuroscience meeting in San Diego in November, 2013

High blood sugar makes Alzheimer’s plaque more toxic

A study of cell cultures taken from rodents’ cerebral blood vessels has found that, while cells exposed to either high glucose or amyloid-beta showed no changes in viability, exposure to both decreased cell viability by 40%. Moreover, cells from diabetic mice were more vulnerable to amyloid-beta, even at normal glucose levels.

The findings support evidence pointing to high glucose as a risk factor for vascular damage associated with Alzheimer’s, and adds weight to the view that controlling blood sugar levels is vital for those with diabetes.

http://www.futurity.org/high-blood-sugar-makes-alzheimers-plaque-toxic/

[3558] Carvalho C, Katz PS, Dutta S, Katakam PVG, Moreira PI, Busija DW. Increased Susceptibility to Amyloid-β Toxicity in Rat Brain Microvascular Endothelial Cells under Hyperglycemic Conditions. Journal of Alzheimer's Disease [Internet]. 2014 ;38(1):75 - 83. Available from: http://dx.doi.org/10.3233/JAD-130464

Mechanism by which diabetes increases Alzheimer's risk revealed

Although it's well-established now that diabetes is a major risk factor for dementia, the reason is still not well understood. To test the hypothesis that epigenetic changes in the brain, affecting synaptic function, may be part of the reason, the brains of diabetics and others were examined post-mortem. Diabetics' brains were found to have significantly higher expression of a class of molecules (histone deacetylases class IIa) and this was associated with impaired expression of synaptic proteins.

This finding was confirmed in mice genetically engineered to develop an Alzheimer’s-type condition, who were induced to develop diabetes. The increase of HDAC IIa was associated with synaptic impairments in the hippocampus, through the work of amyloid oligomers.

Some 60% of Alzheimer's patients have at least one serious medical condition associated with diabetes.

http://www.eurekalert.org/pub_releases/2013-10/tmsh-cie102213.php

[3615] Wang J, Gong B, Zhao W, Tang C, Varghese M, Nguyen T, Bi W, Bilski A, Begum S, Vempati P, et al. Epigenetic Mechanisms Linking Diabetes and Synaptic Impairments. Diabetes [Internet]. 2014 ;63(2):645 - 654. Available from: http://diabetes.diabetesjournals.org/content/63/2/645

High Blood Sugar Linked to Dementia

A seven-year study involving 2,067 older adults (average age 76 at start) has found that those with a high blood glucose level, whether or not they had diabetes, were more likely to develop dementia. Moreover, this was a linear relationship — meaning that the risk steadily increased with higher glucose levels, and decreased the lower it was. Thus, even those with ‘normal’ glucose levels were subject to this relationship, with those whose blood sugar averaged 115 milligrams per deciliter, having an 18% higher risk of dementia than those at 100 mg/dL. Other risk factors, such as high blood pressure, smoking, exercise, and education, were taken into account in the analysis.

The findings add weight to the idea that the brain is a target organ for damage by high blood sugar.

Over the course of the study, a quarter (524) developed dementia of some kind, primarily Alzheimer’s disease or vascular dementia. At the beginning of the study, 232 (11%) had diabetes, and a further 111 developed it by the end of the study. Nearly a third (32%) of those with diabetes at the beginning of the study developed dementia, compared to just under a quarter of those without (24.5%).

http://newoldage.blogs.nytimes.com/2013/08/09/high-blood-sugar-linked-to-dementia/

The journal article is freely available at http://www.nejm.org/doi/full/10.1056/NEJMoa1215740#t=article

[3563] Crane PK, Walker R, Hubbard RA, Li G, Nathan DM, Zheng H, Haneuse S, Craft S, Montine TJ, Kahn SE, et al. Glucose Levels and Risk of Dementia. New England Journal of Medicine [Internet]. 2013 ;369(6):540 - 548. Available from: http://www.nejm.org/doi/full/10.1056/NEJMoa1215740

Undiagnosed pre-diabetes highly prevalent in early Alzheimer's disease

A study involving 128 patients with mild to moderate Alzheimer’s disease, which had specifically excluded those with known diabetes, found that 13% of them did in fact have diabetes, and a further 30% showed glucose intolerance, a pre-diabetic condition.

Turner presented his findings at the Alzheimer's Association International Congress in Boston on July 14.

http://www.eurekalert.org/pub_releases/2013-07/gumc-uph070513.php

Association between hypoglycemia, dementia in older adults with diabetes

A 12-year study involving 783 older adults with diabetes (average age 74) has found that 148 (19%) developed dementia. Those 61 patients (8%) who had a reported hypoglycemic event were twice as likely to develop dementia compared to those who didn’t suffer such an event (34% vs. 17%). Similarly, those with dementia were more likely to experience a severe hypoglycemic event.

The findings suggest some patients risk entering a downward spiral in which hypoglycemia and cognitive impairment fuel one another, leading to worse health

http://www.eurekalert.org/pub_releases/2013-06/tjnj-abh060613.php

http://www.eurekalert.org/pub_releases/2013-06/uoc--aal060613.php

[3622] Yaffe K, CM F, N H, et al. ASsociation between hypoglycemia and dementia in a biracial cohort of older adults with diabetes mellitus. JAMA Internal Medicine [Internet]. 2013 ;173(14):1300 - 1306. Available from: http://dx.doi.org/10.1001/jamainternmed.2013.6176

Dementia risk greatest for older Native-Americans and African-Americans with diabetes

In the first study to look at racial and ethnic differences in dementia risk among older adults with type 2 diabetes, Native Americans were 64% more likely to develop dementia than Asian-Americans, and African-Americans were 44% more likely. Asian-Americans had the lowest risk, and non-Hispanic whites and Latinos were intermediate.

The study involved 22,171 older adults (60+), of whom 3,796 patients (17%) developed dementia over the 10 years of the study. Almost 20% of the African-Americans and Native Americans developed dementia.

The ethnic differences were not explained by diabetes-related complications, glycemic control or duration of diabetes, or neighborhood deprivation index, body mass index, or hypertension.

http://www.eurekalert.org/pub_releases/2013-12/kp-drg121113.php

[3590] Mayeda ER, Karter AJ, Huang ES, Moffet HH, Haan MN, Whitmer RA. Racial/Ethnic Differences in Dementia Risk Among Older Type 2 Diabetic Patients: The Diabetes and Aging Study. Diabetes Care [Internet]. 2014 ;37(4):1009 - 1015. Available from: http://care.diabetesjournals.org/content/37/4/1009

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Physical activity saves hippocampus in people at risk of Alzheimer's

A study involving 97 healthy older adults (65-89) has found that those with the “Alzheimer’s gene” (APOe4) who didn’t engage in much physical activity showed a decrease in hippocampal volume (3%) over 18 months. Those with the gene who did exercise showed no change in the size of their hippocampus, nor did those without the gene, regardless of exercise. Physical activity was classified as low if the participant reported two or fewer days per week of low intensity activity, such as no activity, slow walking or light chores.

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Genes implicated in late-onset Alzheimer's disease

11 new genetic susceptibility factors for Alzheimer’s identified

The largest international study ever conducted on Alzheimer's disease (I-GAP) has identified 11 new genetic regions that increase the risk of late-onset Alzheimer’s, plus 13 other genes yet to be validated. Genetic data came from 74,076 patients and controls from 15 countries.

Eleven genes for Alzheimer's disease have previously been identified.

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Where Alzheimer's starts and how it spreads

A new study involving 96 older adults initially free of dementia at the time of enrollment, of whom 12 subsequently developed mild Alzheimer’s, has clarified three fundamental issues about Alzheimer's: where it starts, why it starts there, and how it spreads.

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