Older news items (pre-2010) brought over from the old website

Neurogenesis improved in Alzheimer mice

Studies of adult neurogenesis in genetically engineered mice have revealed two main reasons why amyloid-beta peptides and apolipoprotein E4 impair neurogenesis, and identified drug treatments that can fix it. The findings point to a deficit in GABAergic neurotransmission or an imbalance between GABAergic and glutamatergic neurotransmission as an important contributor to impaired neurogenesis in Alzheimer’s. While stem cell therapy for Alzheimer’s is still a long way off, these findings are a big step toward that goal.

Gang Li et al. 2009. GABAergic Interneuron Dysfunction Impairs Hippocampal Neurogenesis in Adult Apolipoprotein E4 Knockin Mice. Cell Stem Cell, 5 (6), 634-645.

Binggui Sun et al. 2009. Imbalance between GABAergic and Glutamatergic Transmission Impairs Adult Neurogenesis in an Animal Model of Alzheimer's Disease. Cell Stem Cell, 5 (6), 624-633.

http://www.eurekalert.org/pub_releases/2009-12/gi-gsi113009.php

Mouse study points to possible treatment for chemobrain

A mouse study has found that four commonly used chemotherapy drugs disrupt neurogenesis, and that the condition could be partially reversed with the growth hormone IGF-1. Surprising the researchers, both the drugs which cross the blood-brain barrier (cyclophosphamide and fluorouracil) and the two that don’t (paclitaxel and doxorubicin) reduced neurogenesis, with fluorouracil producing a 15.4% reduction, compared to 22.4% with doxorubicin, 30.5% with cyclophosphamide, 36% with paclitaxel. A second study of a single high dose of cyclophosphamide, a mainstay of breast cancer treatment, resulted in a 40.9% reduction. Administration of the experimental growth hormone IGF-1 helped in all cases, but was more effective with the high dose.

[1472] Janelsins, M. C., Roscoe J. A., Michel J. Berg, Thompson B. D., Gallagher M. J., Morrow G. R., et al.
(2009).  IGF-1 Partially Restores Chemotherapy-Induced Reductions in Neural Cell Proliferation in Adult C57BL/6 Mice.
Cancer Investigation.

http://www.eurekalert.org/pub_releases/2009-12/uorm-usr121709.php

Nerve-cell transplants help brain-damaged rats recover lost ability to learn

After destroying neurons in the subiculum of 48 adult rats, some were given hippocampal cells taken from newborn transgenic mice. On spatial memory tests two months later, the rats given cell transplants performed as well as rats which had not had their subiculums damaged; however, those without transplants had significantly impaired performance. The new cells were found to have mainly settled in the dentate gyrus, where they appeared to promote the secretion of two types of growth factors, namely BDNF and basic fibroblast growth factor (bFGF).

Rekha, J. et al. 2009. Transplantation of hippocampal cell lines restore spatial learning in rats with ventral subicular lesions. Behavioral Neuroscience, 123(6), 1197-1217.

http://www.eurekalert.org/pub_releases/2009-12/apa-nth120909.php

Adult neurogenesis important for discriminating things that are close

A mouse study adds to our understanding of the role of adult neurogenesis — the birth of new brain cells in adults. Mice whose ability to grow new brain cells in the dentate gyrus was removed were able to learn a new location of a food reward in an eight-armed radial maze, but only when the new location was far enough from the original location. This inability to discriminate close locations was confirmed in a touch screen experiment. Computer modeling suggested that this benefit of new neurons might also apply to temporal information, helping us distinguish events occurring closely in time.

[501] Gage, F. H., Bussey T. J., Clelland C. D., Choi M., Romberg C., Clemenson G. D., et al.
(2009).  A Functional Role for Adult Hippocampal Neurogenesis in Spatial Pattern Separation.
Science. 325(5937), 210 - 213.

http://www.eurekalert.org/pub_releases/2009-07/si-nbc070609.php

Baby neurons time-stamp new memories

Since its discovery ten years, adult neurogenesis has been a fruitful area of research, but although we know it’s important for learning and memory, we’re still a little vague on how. Now a new computational model suggests that immature cells are very excitable, easily provoked into firing, while older neurons are more discriminating. The dentate gyrus is designed to separate new memories into separate events (pattern separation), but the indiscriminate excitability of newborn neurons means they link events and memories that happen around the same time (pattern integration) instead. As the brain cells mature, they settle down and join established neural circuits, taking on their proper role, but clusters of neurons that "grew up" around the same time still retain the memories forged in their youth. Which is why independent events that have nothing in common but the fact that they occurred at the same time are connected in our minds: baby neurons have ‘time-stamped’ them.

[785] Aimone, J. B., Wiles J., & Gage F. H.
(2009).  Computational Influence of Adult Neurogenesis on Memory Encoding.
Neuron. 61(2), 187 - 202.

http://www.the-scientist.com/blog/display/55385/
http://www.eurekalert.org/pub_releases/2009-01/si-nbc012209.php

New brain cells are essential for learning

It was only a short time ago that it was accepted wisdom that new neurons were only created during childhood and that being an adult meant facing the gradual death, without replacement, of those neurons. Then, nearly a decade ago, it was discovered that adult brains could create new brain cells, albeit in a very limited way. However, it still hasn’t been clear how important adult neurogenesis is for learning and memory. Now a mouse study makes it clear that in one of the two regions in which neurogenesis takes place, it really is necessary. The study is the first to simultaneously study the two brain regions that produce new neurons, the subventricular zone and the dentate gyrus. Continual cell death was observed in the olfactory bulb, suggesting that newly born neurons (from the subventricular zone) are necessary to take their place. Neurons in the dentate gyrus, however, did not die regularly. However, when neurogenesis was knocked out in the olfactory bulb, no deficits occurred in smell memory, while the same action in the dentate gyrus did result in problems with spatial memory. The findings perhaps open up more questions than they answer — such as how odor memory is maintained when neurons in the olfactory bulb are being continuously replaced.

[1087] Kageyama, R., Imayoshi I., Sakamoto M., Ohtsuka T., Takao K., Miyakawa T., et al.
(2008).  Roles of continuous neurogenesis in the structural and functional integrity of the adult forebrain.
Nat Neurosci. 11(10), 1153 - 1161.

http://www.the-scientist.com/blog/display/54993/
http://www.newscientist.com/channel/being-human/dn14630-new-brain-cells-are-essential-for-learning.html

Injection of human umbilical cord blood helps aging brain

A rat study has found that a single intravenous injection of human umbilical cord blood mononuclear cells in aged rats significantly improved the microenvironment of the aged hippocampus and rejuvenated the aged neural stem/progenitor cells. The increase in neurogenesis seemed to be due to a decrease in inflammation. The results raise the possibility of cell therapy to rejuvenate the aged brain.

[686] Bachstetter, A., Pabon M., Cole M., Hudson C., Sanberg P., Willing A., et al.
(2008).  Peripheral injection of human umbilical cord blood stimulates neurogenesis in the aged rat brain.
BMC Neuroscience. 9(1), 22 - 22.

http://www.physorg.com/news124384387.html

REM sleep deprivation reduces neurogenesis

And in another sleep study, rats deprived of REM sleep for four days showed reduced cell proliferation in the dentate gyrus of the hippocampus, where most adult neurogenesis takes place. The finding indicates that REM sleep is important for brain plasticity.

[507] Guzman-Marin, R., Suntsova N., Bashir T., Nienhuis R., Szymusiak R., & McGinty D.
(2008).  Rapid eye movement sleep deprivation contributes to reduction of neurogenesis in the hippocampal dentate gyrus of the adult rat.
Sleep. 31(2), 167 - 175.

http://www.eurekalert.org/pub_releases/2008-02/aaos-fdo012808.php

Adult neurogenesis confirmed in primates

A study with marmosets has confirmed that the rate at which new neural cells form in the hippocampus (neurogenesis) begins to decline soon after reaching adulthood. This is the first study to confirm the finding from rodent studies in primates, and confirms that findings from rodent studies regarding ways of enhancing adult neurogenesis can be applied to primates.

[1373] Leuner, B., Kozorovitskiy Y., Gross C. G., & Gould E.
(2007).  Diminished adult neurogenesis in the marmoset brain precedes old age.
Proceedings of the National Academy of Sciences. 104(43), 17169 - 17173.

http://www.physorg.com/news111690164.html
http://www.eurekalert.org/pub_releases/2007-10/pu-bcg101207.php

Research explains how lead exposure produces learning deficits

A rat study has shown how exposure to lead during brain development produces learning deficits — by reducing neurogenesis, and by altering the normal development of newly born neurons in the hippocampus. Dendrites (branches from neurons that make the connections with other neurons) were shorter and twisted in lead-exposed rats.

[738] Verina, T., Rohde C. A., & Guilarte T. R.
(2007).  Environmental lead exposure during early life alters granule cell neurogenesis and morphology in the hippocampus of young adult rats.
Neuroscience. 145(3), 1037 - 1047.

http://www.eurekalert.org/pub_releases/2007-04/jhub-reh040307.php

New research shows why too much memory may be a bad thing

People who are able to easily and accurately recall historical dates or long-ago events may have a harder time with word recall or remembering the day's current events. A mouse study reveals why. Neurogenesis has been thought of as a wholly good thing — having more neurons is surely a good thing — but now a mouse study has found that stopping neurogenesis in the hippocampus improved working memory. Working memory is highly sensitive to interference from information previously stored in memory, so it may be that having too much information may hinder performing everyday working memory tasks.

[635] Saxe, M. D., Malleret G., Vronskaya S., Mendez I., Garcia D. A., Sofroniew M. V., et al.
(2007).  Paradoxical influence of hippocampal neurogenesis on working memory.
Proceedings of the National Academy of Sciences. 104(11), 4642 - 4646.

Full text is available at http://www.pnas.org/cgi/reprint/104/11/4642

http://www.physorg.com/news94384934.html
http://www.sciencedaily.com/releases/2007/03/070329092022.htm
http://www.eurekalert.org/pub_releases/2007-03/cumc-nrs032807.php

Sleep deprivation affects neurogenesis

A rat study has found that rats deprived of sleep for 72 hours had higher levels of the stress hormone corticosterone, and produced significantly fewer new brain cells in a particular region of the hippocampus. Preventing corticosterone levels from rising also prevented the reduction in neurogenesis.

[642] Mirescu, C., Peters J. D., Noiman L., & Gould E.
(2006).  Sleep deprivation inhibits adult neurogenesis in the hippocampus by elevating glucocorticoids.
Proceedings of the National Academy of Sciences. 103(50), 19170 - 19175.

http://news.bbc.co.uk/2/hi/health/6347043.stm

Why neurogenesis is so much less in older brains

A rat study has revealed that the aging brain produces progressively fewer new nerve cells in the hippocampus (neurogenesis) not because there are fewer of the immature cells (neural stem cells) that can give rise to new neurons, but because they divide much less often. In young rats, around a quarter of the neural stem cells were actively dividing, but only 8% of cells in middle-aged rats and 4% in old rats were. This suggests a new approach to improving learning and memory function in the elderly.

[1077] Hattiangady, B., & Shetty A. K.
(2008).  Aging does not alter the number or phenotype of putative stem/progenitor cells in the neurogenic region of the hippocampus.
Neurobiology of Aging. 29(1), 129 - 147.

http://www.eurekalert.org/pub_releases/2006-12/dumc-sca121806.php

Neurogenesis not the sole cause of enriched environment effects

The creation of new neurons in the hippocampus (adult neurogenesis) and improved cognitive function have been repeatedly found in tandem with a more stimulating environment, and it’s been assumed that the improvement in cognitive function has resulted from the neurogenesis. However, a new study has produced the startling finding that if neurogenesis is prevented, an enriched environment still produces improved spatial memory skills and less anxiety in mice. This doesn't mean adult neurogenesis plays no role, but it does indicate that neurogenesis is not the whole story.

[601] Meshi, D., Drew M. R., Saxe M., Ansorge M. S., David D., Santarelli L., et al.
(2006).  Hippocampal neurogenesis is not required for behavioral effects of environmental enrichment.
Nat Neurosci. 9(6), 729 - 731.

http://sciencenow.sciencemag.org/cgi/content/full/2006/503/1?etoc

Losing sleep inhibits neurogenesis

A new sleep study using rats restricted rather than deprived them of sleep, to mimic more closely the normal human experience. The study found that the sleep-restricted rats had a harder time remembering a path through a maze compared to their rested counterparts. The sleep-restricted rats showed reduced survival rate of new hippocampus cells — learning spatial tasks increases the production of new cells in the hippocampus. This study shows that sleep plays a part in helping those new brain cells survive. However, the sleep-restricted rats that were forced to use visual and odor cues to remember their way through the maze did better on the task than their rested counterparts, implying that some types of learning don’t require sleep.

[994] Hairston, I. S., Little M. T. M., Scanlon M. D., Barakat M. T., Palmer T. D., Sapolsky R. M., et al.
(2005).  Sleep Restriction Suppresses Neurogenesis Induced by Hippocampus-Dependent Learning.
J Neurophysiol. 94(6), 4224 - 4233.

http://www.eurekalert.org/pub_releases/2006-01/aps-lsu010506.php

Fitness counteracts cognitive decline from hormone-replacement therapy

A study of 54 postmenopausal women (aged 58 to 80) suggests that being physically fit offsets cognitive declines attributed to long-term hormone-replacement therapy. It was found that gray matter in four regions (left and right prefrontal cortex, left parahippocampal gyrus and left subgenual cortex) was progressively reduced with longer hormone treatment, with the decline beginning after more than 10 years of treatment. Therapy shorter than 10 years was associated with increased tissue volume. Higher fitness scores were also associated with greater tissue volume. Those undergoing long-term hormone therapy had more modest declines in tissue loss if their fitness level was high. Higher fitness levels were also associated with greater prefrontal white matter regions and in the genu of the corpus callosum. The findings need to be replicated with a larger sample, but are in line with animal studies finding that estrogen and exercise have similar effects: both stimulate brain-derived neurotrophic factor.

[375] Erickson, K. I., Colcombe S. J., Elavsky S., McAuley E., Korol D. L., Scalf P. E., et al.
(2007).  Interactive effects of fitness and hormone treatment on brain health in postmenopausal women.
Neurobiology of Aging. 28(2), 179 - 185.

http://www.eurekalert.org/pub_releases/2006-01/uoia-fcc012406.php

Immune function important for cognition

New research overturns previous beliefs that immune cells play no part in — and may indeed constitute a danger to — the brain. Following on from an earlier study that suggested that T cells — immune cells that recognize brain proteins — have the potential to fight off neurodegenerative conditions such as Alzheimer’s, researchers have found that neurogenesis in adult rats kept in stimulating environments requires these immune cells. A further study found that mice with these T cells performed better at some tasks than mice lacking the cells. The researchers suggest that age-related cognitive decline may be related to this, as aging is associated with a decrease in immune system function, suggesting that boosting the immune system may also benefit cognitive function in older adults.

[435] Ziv, Y., Ron N., Butovsky O., Landa G., Sudai E., Greenberg N., et al.
(2006).  Immune cells contribute to the maintenance of neurogenesis and spatial learning abilities in adulthood.
Nat Neurosci. 9(2), 268 - 275.

http://www.eurekalert.org/pub_releases/2006-01/acft-wis011106.php

How new neurons are integrated in the adult brain

Now that we accept that new neurons can indeed be created in adult brains, the question becomes: how are these new neurons integrated into existing networks? Mouse experiments have now found that a brain chemical called GABA is critical. Normally, GABA inhibits neuronal signals, but it turns out that with new neurons, GABA has a different effect: it excites them, and prepares them for integration into the adult brain. Thus a constant flood of GABA is needed initially; the flood then shifts to a more targeted pulse that gives the new neuron specific connections that communicate using GABA; finally, the neuron receives connections that communicate via another chemical, glutamate. The neuron is now ready to function as an adult neuron, and will respond to glutamate and GABA as it should. It’s hoped the discovery will help efforts to increase neuron regeneration in the brain or to make transplanted stem cells form connections more efficiently.

[237] Ge, S., Goh E. L. K., Sailor K. A., Kitabatake Y., Ming G-li., & Song H.
(2006).  GABA regulates synaptic integration of newly generated neurons in the adult brain.
Nature. 439(7076), 589 - 593.

http://www.eurekalert.org/pub_releases/2005-12/jhmi-nnt122205.php

Neuron growth in adult brain

A few years ago, we were surprised by news that new neurons could be created in the adult brain. However, it’s remained a tenet that adult neurons don’t grow — this because researchers have found no sign that any structural remodeling takes place in an adult brain. Now a mouse study using new techniques has revealed that dramatic restructuring occurs in the less-known, less-accessible inhibitory interneurons. Dendrites (the branched projections of a nerve cell that conducts electrical stimulation to the cell body) show sometimes dramatic growth, and this growth is tied to use, supporting the idea that the more we use our minds, the better they will be. The finding also offers new hope that one day it may be possible to grow new cells to replace ones damaged by disease or spinal cord injury.

Lee, W.C.A., Huang, H., Feng, G., Sanes, J.R., Brown, E.N. et al. 2006. Dynamic remodeling of dendritic arbors in GABAergic interneurons of adult visual cortex. PLoS Biol 4(2): e29.

Full text available at http://www.plosbiology.org/article/info:doi/10.1371/journal.pbio.0040042

http://www.eurekalert.org/pub_releases/2005-12/miot-mrf122205.php
http://www.eurekalert.org/pub_releases/2005-12/plos-anw122205.php

More light on adult neurogenesis; implications for dementia and brain injuries

New research has demonstrated that adult mice produce multi-purpose, or progenitor, cells in the hippocampus, and indicates that the stem cells ultimately responsible for adult hippocampal neurogenesis actually reside outside the hippocampus, producing progenitor cells that migrate into the neurogenic zones and proliferate to produce new neurons and glia. The finding may help in the development of repair mechanisms for people suffering from dementia and acquired brain injury.

[977] Bull, N. D., & Bartlett P. F.
(2005).  The Adult Mouse Hippocampal Progenitor Is Neurogenic But Not a Stem Cell.
J. Neurosci.. 25(47), 10815 - 10821.

http://www.eurekalert.org/pub_releases/2005-11/ra-nrt112305.php

Wnt signaling vital for adult neurogenesis

Neurogenesis (the birth of new neurons) only occurs in adult brains in two areas: the lateral ventricle, and the dentate gyrus (in the hippocampus). New neurons are spawned from the division of stem cells — but how do they decide whether to remain a stem cell, turn into a neuron, or a support cell (an astrocyte or oligodendrocyte)? A new study has pinpointed the protein that provides a vital chemical signal that helps this decision in the hippocampus. When Wnt3 proteins were blocked in the brains of adult mice, neurogenesis decreased dramatically; when additional Wnt3 was introduced, neurogenesis increased. Wnt3 molecules are secreted by astrocytes.

[537] Dearie, A. R., Gage F. H., Lie D-C., Colamarino S. A., Song H-J., Desire L., et al.
(2005).  Wnt signalling regulates adult hippocampal neurogenesis.
Nature. 437(7063), 1370 - 1375.

http://www.eurekalert.org/pub_releases/2005-10/si-wsc102405.php

Why premature brains improve over time

A new study explains why premature babies often develop better than expected. A mouse study has found that infants born prematurely and with hypoxia (inadequate oxygen to the blood) are able to recover some cells, volume and weight in the brain after oxygen supply is restored, by a process of neurogenesis.

[1402] Fagel, D. M., Ganat Y., Silbereis J., Ebbitt T., Stewart W., Zhang H., et al.
(2006).  Cortical neurogenesis enhanced by chronic perinatal hypoxia.
Experimental Neurology. 199(1), 77 - 91.

http://www.eurekalert.org/pub_releases/2005-06/yu-gsh062705.php

One gene links neurogenesis with neurodegenerative diseases such as Alzheimer's

It used to be thought that the neurons we were born with (or created soon after birth) were all that we could ever have. Then it was discovered that certain neurons in specific brain regions, could be created in an adult brain (neurogenesis). A recent study has investigated the question of what’s different about these neurons, and to the researchers’ surprise, has discovered that replaceable neurons differed from unreplaceable neurons by having persistently low levels of a particular gene known as UCHL1. Intriguingly, UCHL1, expressed as a protein in high quantities throughout the brain, has also been identified as being deficient in degenerative diseases such as Alzheimer's and Parkinson's. Further research revealed that behavior that increases the chance of new neurons surviving is also associated with increases in the level of UCHL1 in replaceable neurons. The findings suggest that rising levels of UCHL1 may be associated with a reduced risk of neuronal death.

[336] Lombardino, A. J., Li X-C., Hertel M., & Nottebohm F.
(2005).  Replaceable neurons and neurodegenerative disease share depressed UCHL1 levels.
Proceedings of the National Academy of Sciences of the United States of America. 102(22), 8036 - 8041.

http://www.eurekalert.org/pub_releases/2005-05/ru-ogl052005.php

Social status influences brain structure

A rat study has found that dominant rats have more new nerve cells in the hippocampus than their subordinates, suggesting that social hierarchies can influence brain structure. Seven colonies of 6 rats (4 male and 2 female) established their pecking order within three days, and were tested two weeks later. The dominant males had some 30% more neurons in their dentate gyrus than both the subordinate rats and controls. The increase seems to be because the new cells constantly being born in this area of the brain (most of which usually die within a week) were surviving longer. Hippocampal neurons have already been shown to be responsive to negative factors such as stress, and positive factors such as exercise and environmental enrichment. The increase in neurons was maintained when the rats were removed from the social setting.

[372] Kozorovitskiy, Y., & Gould E.
(2004).  Dominance Hierarchy Influences Adult Neurogenesis in the Dentate Gyrus.
J. Neurosci.. 24(30), 6755 - 6759.

http://www.nature.com/news/2004/040802/full/040802-18.html

Learning involves the death of neurons too

When we think about learning at the neural level, it is always the birth of new neurons and new synaptic connections that is thought of. Now it appears that death is involved too. A recent rat study has found that while new cells are being generated in the hippocampus, other cells are dying off. The study distinguished two phases of learning during a water maze task: the first phase, when the rat learns to navigate the maze; and the second phase, when the learned behavior is refined. During the second phase, it appears, new cells are born in the dentate gyrus, while some of the cells that were born during the first phase, disappear. If true, this could be "a trimming mechanism that suppresses neurons that have not established learning-related synaptic connections."

[724] Dobrossy, M. D., Drapeau E., Aurousseau C., Le Moal M., Piazza P. V., & Abrous D. N.
(0).  Differential effects of learning on neurogenesis: learning increases or decreases the number of newly born cells depending on their birth date.
Mol Psychiatry. 8(12), 974 - 982.

http://www.eurekalert.org/pub_releases/2003-11/mp-cdp112103.php

FGF-2 implicated in adult neurogenesis

The whole question of neurogenesis (the making of new neurons) in the adult brain has been much debated – does neurogenesis happen? how does it happen? how much does it happen? Well, recent research has appeared to answer the first question – yes, neurogenesis does happen in the adult brain – and now a new study provides some clarification about the mechanism. Experiments with a special strain of laboratory-bred mice indicate that fibroblast growth factor-2 (FGF-2) is at least partly responsible for regulating the replacement of neurons, and suggest that supplementation with FGF-2 might be a beneficial strategy for those suffering traumatic brain injury, by both enhancing neurogenesis and reducing neurodegeneration.

[887] Moskowitz, M. A., Yoshimura S., Teramoto T., Whalen M. J., Irizarry M. C., Takagi Y., et al.
(2003).  FGF-2 regulates neurogenesis and degeneration in the dentate gyrus after traumatic brain injury in mice.
Journal of Clinical Investigation. 112(8), 1202 - 1210.

http://www.biomedcentral.com/news/20031016/03

Too much exercise may be bad for the brain

Mice bred for 30 generations to display increased voluntary wheel running behavior – an "exercise addiction" – showed much higher amounts of BDNF (brain-derived neurotrophic factor – a chemical involved in protecting and producing neurons in the hippocampus) than normal, sedentary mice. In a related study, it was found that the mice also grow more neurons there as well. However, while BDNF and neurogenesis are good for learning and memory, this doesn’t necessarily mean an exercise addict learns at a faster rate. The “running addict” mice in fact performed much worse than normal mice when attempting to navigate around a maze. It could be that too much BDNF and neuron production may be a bad thing, or it may be that the hyperactive wheel running exercise actually kills or damages neurons in the hippocampus, and the high BDNF production is simply trying to minimize this damage. At the moment, all we can say with surety is that exercise greatly activates the hippocampus.

[747] Johnson, R. A., Rhodes J. S., Jeffrey S. L., Garland T., & Mitchell G. S.
(2003).  Hippocampal brain-derived neurotrophic factor but not neurotrophin-3 increases more in mice selected for increased voluntary wheel running.
Neuroscience. 121(1), 1 - 7.

[504] Rhodes, J. S., van Praag H., Jeffrey S., Girard I., Mitchell G. S., Garland, Theodore J., et al.
(2003).  Exercise increases hippocampal neurogenesis to high levels but does not improve spatial learning in mice bred for increased voluntary wheel running..
Behavioral Neuroscience. 117(5), 1006 - 1016.

http://www.eurekalert.org/pub_releases/2003-09/ohs-cn092603.php

Rat studies provide more evidence on why aging can impair memory

Among aging rats, those that have difficulty navigating water mazes have no more signs of neuron damage or cell death in the hippocampus, a brain region important in memory, than do rats that navigate with little difficulty. Nor does the extent of neurogenesis (birth of new cells in an adult brain) seem to predict poorer performance. Although the researchers have found no differences in a variety of markers for postsynaptic signals between elderly rats with cognitive impairment and those without, decreases in a presynaptic signal are correlated with worse cognitive impairment. That suggests that neurons in the impaired rat brains may not be sending signals correctly.

Gallagher, M. 2002. Markers for memory decline. Paper presented at the Society for Neuroscience annual meeting in Orlando, Florida, 5 November

New neurons in adult brains are functional

Following studies indicating that new neurons are generated in the adult mammalian hippocampus, this study demonstrates that these newly generated cells do mature into functional neurons.

[590] van Praag, H., Schinder A. F., Christie B. R., Toni N., Palmer T. D., & Gage F. H.
(2002).  Functional neurogenesis in the adult hippocampus.
Nature. 415(6875), 1030 - 1034.

Living in large groups could give you a better memory

A study into the brains of songbirds found that birds living in large groups have more new neurons and probably a better memory than those living alone. Does this have relevance for humans? We don't know yet, but it has been observed that social animals such as elephants tend to have better memories than loners.

[774] Lipkind, D., Nottebohm F., Rado R., & Barnea A.
(2002).  Social change affects the survival of new neurons in the forebrain of adult songbirds.
Behavioural Brain Research. 133(1), 31 - 43.

http://www.eurekalert.org/pub_releases/2002-02/ns-lil022002.php

http://www.newscientist.com/article/mg17323312.700-the-brainy-bunch.html

New study contradicts earlier finding of new brain cell growth in the adult primate neocortex

A very exciting finding a couple of years ago, was that adult monkeys were found to be able to create new neurons in the neocortex, the most recently evolved part of the brain. However a new study, using the most sophisticated cell analysis techniques available to analyze thousands of cells in the neocortex, has found that those neurons that appear to be new are in fact two separate cells, usually one “old” neuron and one newly created cell of a different type, such as a glial cell — although new neurons were indeed found in the hippocampus and the olfactory bulb (both older parts of the brain).

[208] Kornack, D. R., & Rakic P.
(2001).  Cell Proliferation Without Neurogenesis in Adult Primate Neocortex.
Science. 294(5549), 2127 - 2130.

http://www.eurekalert.org/pub_releases/2001-12/uorm-std120601.php

BDNF

BDNF is involved in protecting and producing neurons in the hippocampus. higher levels of BDNF are associated with higher levels of neurogenesis. Neurotrophins are molecules that function in the survival, growth and migration of neurons

Nerve-cell transplants help brain-damaged rats recover lost ability to learn

After destroying neurons in the subiculum of 48 adult rats, some were given hippocampal cells taken from newborn transgenic mice. On spatial memory tests two months later, the rats given cell transplants performed as well as rats which had not had their subiculums damaged; however, those without transplants had significantly impaired performance. The new cells were found to have mainly settled in the dentate gyrus, where they appeared to promote the secretion of two types of growth factors, namely BDNF and basic fibroblast growth factor (bFGF).

Rekha, J. et al. 2009. Transplantation of hippocampal cell lines restore spatial learning in rats with ventral subicular lesions. Behavioral Neuroscience, 123(6), 1197-1217.

http://www.eurekalert.org/pub_releases/2009-12/apa-nth120909.php

Exercise may counteract bad effect of high-fat diet on memory

An animal study has investigated the interaction of diet and exercise on synaptic plasticity (an important factor in learning performance). A diet high in fat reduced levels of brain-derived neurotrophic factor (BDNF) in the hippocampus, and impaired performance on spatial learning tasks, but both of these consequences were prevented in those animals with access to voluntary wheel-running. Exercise appeared to interact with the same molecular systems disrupted by the high-fat diet.

[883] Molteni, R., Wu A., Vaynman S., Ying Z., Barnard R. J., & Gómez-Pinilla F.
(2004).  Exercise reverses the harmful effects of consumption of a high-fat diet on synaptic and behavioral plasticity associated to the action of brain-derived neurotrophic factor.
Neuroscience. 123(2), 429 - 440.

Too much exercise may be bad for the brain

Mice bred for 30 generations to display increased voluntary wheel running behavior – an "exercise addiction" – showed much higher amounts of BDNF (brain-derived neurotrophic factor – a chemical involved in protecting and producing neurons in the hippocampus) than normal, sedentary mice. In a related study, it was found that the mice also grow more neurons there as well. However, while BDNF and neurogenesis are good for learning and memory, this doesn’t necessarily mean an exercise addict learns at a faster rate. The “running addict” mice in fact performed much worse than normal mice when attempting to navigate around a maze. It could be that too much BDNF and neuron production may be a bad thing, or it may be that the hyperactive wheel running exercise actually kills or damages neurons in the hippocampus, and the high BDNF production is simply trying to minimize this damage. At the moment, all we can say with surety is that exercise greatly activates the hippocampus.

Johnson, R.A., Rhodes, J.S., Jeffrey, S.L., Garland, T. Jr., & Mitchell, G.S. 2003. Hippocampal brain-derived neurotrophic factor but not neurotrophin-3 increases more in mice selected for increased voluntary wheel running. Neuroscience, 121 (1), 1-7.

Rhodes, J.S., van Praag, H., Jeffrey, S., Girard, I., Mitchell, G.S., Garland, T. Jr., & Gage, F.H. 2003. Exercise Increases Hippocampal Neurogenesis to High Levels but Does Not Improve Spatial Learning in Mice Bredfor Increased Voluntary Wheel Running. Behavioral Neuroscience, 117 (5), 1006–1016.

http://www.eurekalert.org/pub_releases/2003-09/ohs-cn092603.php

Meal skipping protects the nerve cells of mice

Further to the study reported in January, a new mouse study suggests fasting every other day may protect brain neurons as well as or better than either vigorous exercise or caloric restriction. The mice were allowed to eat as much as they wanted on non-fasting days, and did not, overall, eat fewer calories than the control group. Their nerve cells however, proved to be more resistant to neurotoxin injury or death than nerve cells of both the calorie-restricted mice or the control group. Previous research has found that meal-skipping diets can stimulate brain cells in mice to produce a protein called brain-derived neurotrophic factor (BDNF) that promotes the survival and growth of nerve cells. The researchers are now investigating the effects of meal-skipping on the cardiovascular system in laboratory rats.

[1429] Anson, M. R., Guo Z., de Cabo R., Iyun T., Rios M., Hagepanos A., et al.
(2003).  Intermittent fasting dissociates beneficial effects of dietary restriction on glucose metabolism and neuronal resistance to injury from calorie intake.
Proceedings of the National Academy of Sciences of the United States of America. 100(10), 6216 - 6220.

http://www.eurekalert.org/pub_releases/2003-04/nioa-msh042403.php

Gene linked to poor episodic memory

Brain derived neurotrophic factor (BDNF) plays a key role in neuron growth and survival and, it now appears, memory. We inherit two copies of the BDNF gene - one from each parent - in either of two versions. Slightly more than a third inherit at least one copy of a version nicknamed "met," which the researchers have now linked to poorer memory. Those who inherit the “met” gene appear significantly worse at remembering events that have happened to them, probably as a result of the gene’s effect on hippocampal function. Most notably, those who had two copies of the “met” gene scored only 40% on a test of episodic (event) memory, while those who had two copies of the other version scored 70%. Other types of memory did not appear to be affected. It is speculated that having the “met” gene might also increase the risk of disorders such as Alzheimer’s and Parkinsons.

[1039] Dean, M., Egan M. F., Kojima M., Callicott J. H., Goldberg T. E., Kolachana B. S., et al.
(2003).  The BDNF val66met Polymorphism Affects Activity-Dependent Secretion of BDNF and Human Memory and Hippocampal Function.
Cell. 112(2), 257 - 269.

http://www.eurekalert.org/pub_releases/2003-01/niom-hga012203.php
http://news.bbc.co.uk/1/hi/health/2687267.stm