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The Tip of the Tongue State
This book brings together the body of empirical findings and theoretical interpretations of the tip of the tongue (TOT) experience - when a well-known or familiar word cannot immediately be recalled. Although research has been published on TOTs for over a century, the experience retains its fascination for both cognitive and linguistic researchers.
After a review of various research procedures used to study TOTs, the book offers a summary of attempts to manipulate this rare cognitive experience through cue and prime procedures. Various aspects of the inaccessible target word are frequently available - such as first letter and syllable number - even in the absence of actual retrieval, and the book explores the implications of these bits of target-word information for mechanisms for word storage and retrieval. It also examines: what characteristics of a word make it potentially more vulnerable to a TOT; why words related to the target word (called \"interlopers\") often come to mind; the recovery process, when the momentarily-inaccessible word is recovered shortly after the TOT is first experienced; and efforts to evaluate individual differences in the likelihood to experience TOTs.
eBook
Memory in autism : theory and evidence
Many people with autism spectrum disorders (ASD) are remarkably proficient at remembering how things look and sound and are good at rote learning. However, all ASD sufferers have poor ability to recall personal memories and relive experiences. This book assembles research to examine why this happens and the effects it has.
BOOK
Myelin degeneration and diminished myelin renewal contribute to age-related deficits in memory
Cognitive decline remains an unaddressed problem for the elderly. We show that myelination is highly active in young mice and greatly inhibited in aged mice, coinciding with spatial memory deficits. Inhibiting myelination by deletion of Olig2 in oligodendrocyte precursor cells impairs spatial memory in young mice, while enhancing myelination by deleting the muscarinic acetylcholine receptor 1 in oligodendrocyte precursor cells, or promoting oligodendroglial differentiation and myelination via clemastine treatment, rescues spatial memory decline during aging.Wang et al. show that myelination is greatly inhibited in aged brains. Enhancing myelination by ablation of M1R in OPCs or clemastine treatment promotes oligodendroglial differentiation and consequently rescues spatial memory decline during aging.
Journal Article
Memory activity book : engaging ways to stimulate the brain, for people living with memory loss or dementia
More than 70 brain-stimulating activities for people with memory loss or dementia, including Alzheimer's disease. Physical and mental activities along with social interaction may help maintain your brain health and slow the progress of memory loss and dementia, including Alzheimer's disease. They can also provide a meaningful way to connect. This book is packed with fun and creative ideas, from nature walks, gardening, and exercise to arts, crafts, puzzles, and games. Each activity includes step-by-step instructions, the specific benefits, and ways to adapt the activity for different abilities. Designed for people with memory loss or dementia along with their family, friends, and caregivers, AARP's Memory Activity Book is a valuable resource for everyone touched by these conditions.
Book
Caspase-1 inhibition alleviates cognitive impairment and neuropathology in an Alzheimer’s disease mouse model
Alzheimer's disease (AD) is an intractable progressive neurodegenerative disease characterized by cognitive decline and dementia. An inflammatory neurodegenerative pathway, involving Caspase-1 activation, is associated with human age-dependent cognitive impairment and several classical AD brain pathologies. Here, we show that the nontoxic and blood–brain barrier permeable small molecule Caspase-1 inhibitor VX-765 dose-dependently reverses episodic and spatial memory impairment, and hyperactivity in the J20 mouse model of AD. Cessation of VX-765 results in the reappearance of memory deficits in the mice after 1 month and recommencement of treatment re-establishes normal cognition. VX-765 prevents progressive amyloid beta peptide deposition, reverses brain inflammation, and normalizes synaptophysin protein levels in mouse hippocampus. Consistent with these findings, Caspase-1 null J20 mice are protected from episodic and spatial memory deficits, neuroinflammation and Aβ accumulation. These results provide in vivo proof of concept for Caspase-1 inhibition against AD cognitive deficits and pathologies.
Caspase-1, activated by stress in immune cells and in CNS human neurons, may contribute to neuronal degeneration. Here, the authors investigate the therapeutic potential of a Caspase-1 inhibitor in a mouse model of Alzheimer’s disease.
Journal Article
One week friends. 5
Hearing Hajime's story about the friendship he once shared with Kaori leads Yuuki to help reunite the pair. With a new old friend now in the mix, Kaori needs more than one diary to avoid starting every week from zero. But when Hajime and Kaori start to display a special bond that can be shared only by longtime friends, Yuuki is forced to wonder exactly what sort of relationship he wants with someone whose memory of him lasts only so long ...
Book
A complement–microglial axis drives synapse loss during virus-induced memory impairment
People infected with West Nile virus often experience cognitive side effects including memory loss through unknown mechanisms; mice and humans infected with the virus experience a loss in hippocampal presynaptic terminals, which can be reversed by disrupting complement or microglia in mice.
Cognitive abnormalities associated with West Nile virus
A majority of West Nile virus (WNV) sufferers experience cognitive signs and symptoms, including memory dysfunction, but the mechanisms driving these impairments are largely unknown. Robyn Klein and colleagues demonstrate an enhancement of complement-mediated synaptic pruning in the hippocampus following WNV infection. This pruning required microglia and resembled developmental pruning by the same mechanism. Disruption of complement or microglia during infection protected animals from the WNV-induced memory deficits.
Over 50% of patients who survive neuroinvasive infection with West Nile virus (WNV) exhibit chronic cognitive sequelae
1
,
2
. Although thousands of cases of WNV-mediated memory dysfunction accrue annually
3
, the mechanisms responsible for these impairments are unknown. The classical complement cascade, a key component of innate immune pathogen defence, mediates synaptic pruning by microglia during early postnatal development
4
,
5
. Here we show that viral infection of adult hippocampal neurons induces complement-mediated elimination of presynaptic terminals in a murine WNV neuroinvasive disease model. Inoculation of WNV-NS5-E218A, a WNV with a mutant NS5(E218A) protein
6
,
7
leads to survival rates and cognitive dysfunction that mirror human WNV neuroinvasive disease. WNV-NS5-E218A-recovered mice (recovery defined as survival after acute infection) display impaired spatial learning and persistence of phagocytic microglia without loss of hippocampal neurons or volume. Hippocampi from WNV-NS5-E218A-recovered mice with poor spatial learning show increased expression of genes that drive synaptic remodelling by microglia via complement. C1QA was upregulated and localized to microglia, infected neurons and presynaptic terminals during WNV neuroinvasive disease. Murine and human WNV neuroinvasive disease post-mortem samples exhibit loss of hippocampal CA3 presynaptic terminals, and murine studies revealed microglial engulfment of presynaptic terminals during acute infection and after recovery. Mice with fewer microglia (
Il34
−/−
mice with a deficiency in IL-34 production) or deficiency in complement C3 or C3a receptor were protected from WNV-induced synaptic terminal loss. Our study provides a new murine model of WNV-induced spatial memory impairment, and identifies a potential mechanism underlying neurocognitive impairment in patients recovering from WNV neuroinvasive disease.
Journal Article
NK3
\"In post-NK3 Los Angeles, a sixty-foot-tall fence surrounds the hills where the rich used to live, but the mansions have been taken over by those with the only power that matters: the power of memory. Life for the community inside the Fence, ruled over by the new aristocracy, the Verified, is a perpetual party. Outside the Fence, in downtown Los Angeles, the Verified use an invented mythology to keep control over the mindless and nameless Drifters, Shamblers, and Bottle Bangers who serve the gift economy until no longer needed. The ruler, Chief, takes his guidance from gigantic effigies of a man and a woman in the heart of the Fence\"-- Provided by publisher.
Book
A cannabinoid link between mitochondria and memory
Cannabinoids affect CB
1
receptors on the mitochondrial membranes in the brain, triggering a decrease in downstream cAMP-dependent signalling; this leads to a decrease in brain mitochondrial activity and to cannabinoid-induced amnesia.
Bioenergetics deficiency and memory
The pathological effect of chronic mitochondrial dysfunction on cognitive function is well established, however the acute modulation of neural processing by mitochondrial signalling is less well understood. These authors demonstrate that acute functional disruption of the brain by cannabinoids involves the activation and signalling from mitochondrial cannabinoid receptors. Thus, even acute mitochondrial bioenergetic changes or disruption can have a short-term effect on cognition, underscoring the role that mitochondria have in regulating normal brain activity.
Cellular activity in the brain depends on the high energetic support provided by mitochondria, the cell organelles which use energy sources to generate ATP
1
,
2
,
3
,
4
. Acute cannabinoid intoxication induces amnesia in humans and animals
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,
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, and the activation of type-1 cannabinoid receptors present at brain mitochondria membranes (mtCB
1
) can directly alter mitochondrial energetic activity
7
,
8
,
9
. Although the pathological impact of chronic mitochondrial dysfunctions in the brain is well established
1
,
2
, the involvement of acute modulation of mitochondrial activity in high brain functions, including learning and memory, is unknown. Here, we show that acute cannabinoid-induced memory impairment in mice requires activation of hippocampal mtCB
1
receptors. Genetic exclusion of CB
1
receptors from hippocampal mitochondria prevents cannabinoid-induced reduction of mitochondrial mobility, synaptic transmission and memory formation. mtCB
1
receptors signal through intra-mitochondrial Gα
i
protein activation and consequent inhibition of soluble-adenylyl cyclase (sAC). The resulting inhibition of protein kinase A (PKA)-dependent phosphorylation of specific subunits of the mitochondrial electron transport system eventually leads to decreased cellular respiration. Hippocampal inhibition of sAC activity or manipulation of intra-mitochondrial PKA signalling or phosphorylation of the Complex I subunit NDUFS2 inhibit bioenergetic and amnesic effects of cannabinoids. Thus, the G protein-coupled mtCB
1
receptors regulate memory processes via modulation of mitochondrial energy metabolism. By directly linking mitochondrial activity to memory formation, these data reveal that bioenergetic processes are primary acute regulators of cognitive functions.
Journal Article