88-year-old George H.W. Bush: "maybe you come out with a new drug that makes memory to come roaring back"

Former President George H.W. Bush wrote a poem for her grandchildren:

"so I can add the relationship on getting older.

Who knows, maybe you come out with a new drug that makes your legs bend easier,
Joints of the lesser evil, to go beyond, come roaring back, memory
And all fears of falling rocks fishing going on. 

Remember an old song: I'll be ready when you are.
Well I'll be ready when you are
There is so much excitement ahead, many grandchildren watch grow.
If you need me I'm here. "

By the way, the former President, 88-year-old said he wasn't done skydiving. His goal: to jump again when he is 90.
References:

' If you need me I'll be there ': George H.w. Bush moved to tears during the interview with granddaughter Jenna on her old family and growing | Daily Mail Online http://goo.gl/noCt0

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88-year-old George H.W. Bush: "maybe you come out with a new drug that makes memory to come roaring back"

Former President George H.W. Bush wrote a poem for her grandchildren:

"so I can add the relationship on getting older.

Who knows, maybe you come out with a new drug that makes your legs bend easier,
Joints of the lesser evil, to go beyond, come roaring back, memory
And all fears of falling rocks fishing going on. 

Remember an old song: I'll be ready when you are.
Well I'll be ready when you are
There is so much excitement ahead, many grandchildren watch grow.
If you need me I'm here. "

By the way, the former President, 88-year-old said he wasn't done skydiving. His goal: to jump again when he is 90.
References:

' If you need me I'll be there ': George H.w. Bush moved to tears during the interview with granddaughter Jenna on her old family and growing | Daily Mail Online http://goo.gl/noCt0

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Sleep-dependent memory consolidation in patients with sleep disorders

Sleep can improve the off-line memory consolidation of new items of declarative and non-declarative information in healthy subjects, whereas acute sleep loss, as well as sleep restriction and fragmentation, impair consolidation. This suggests that, by modifying the amount and/or architecture of sleep, chronic sleep disorders may also lead to a lower gain in off-line consolidation, which in turn may be responsible for the varying levels of impaired performance at memory tasks usually observed in sleep-disordered patients.

The experimental studies conducted to date have shown specific impairments of sleep-dependent consolidation overall for verbal and visual declarative information in patients with primary insomnia, for verbal declarative information in patients with obstructive sleep apnoeas, and for visual procedural skills in patients with narcolepsy-cataplexy.

These findings corroborate the hypothesis that impaired consolidation is a consequence of the chronically altered organization of sleep. Moreover, they raise several novel questions as to: a) the reversibility of consolidation impairment in the case of effective treatment, b) the possible negative influence of altered prior sleep also on the encoding of new information, and c) the relationships between altered sleep and memory impairment in patients with other (medical, psychiatric or neurological) diseases associated with quantitative and/or qualitative changes of sleep architecture.

Table 1. Methodological characteristics and results of the experimental studies on memory consolidation during sleep in patients with chronic sleep disorders.

Abbreviations: DM = declarative memory; NC = narcolepsy with cataplexy; NDM = non declarative memory; OSA = obstructive sleep apnoea; PI = primary insomnia; REM = rapid eye movement (sleep); REMD = REM density; SE = sleep efficiency; SWS = slow wave sleep; SPT = sleep period time; SFI = sleep fragmentation index; SOA= stimulus onset asynchrony; TST = total sleep time; WASO = wake after sleep onset.

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Copyright © 2012 Elsevier Ltd. All rights reserved.

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Sleep-dependent memory consolidation in patients with sleep disorders

Sleep can improve the off-line memory consolidation of new items of declarative and non-declarative information in healthy subjects, whereas acute sleep loss, as well as sleep restriction and fragmentation, impair consolidation. This suggests that, by modifying the amount and/or architecture of sleep, chronic sleep disorders may also lead to a lower gain in off-line consolidation, which in turn may be responsible for the varying levels of impaired performance at memory tasks usually observed in sleep-disordered patients.

The experimental studies conducted to date have shown specific impairments of sleep-dependent consolidation overall for verbal and visual declarative information in patients with primary insomnia, for verbal declarative information in patients with obstructive sleep apnoeas, and for visual procedural skills in patients with narcolepsy-cataplexy.

These findings corroborate the hypothesis that impaired consolidation is a consequence of the chronically altered organization of sleep. Moreover, they raise several novel questions as to: a) the reversibility of consolidation impairment in the case of effective treatment, b) the possible negative influence of altered prior sleep also on the encoding of new information, and c) the relationships between altered sleep and memory impairment in patients with other (medical, psychiatric or neurological) diseases associated with quantitative and/or qualitative changes of sleep architecture.

Table 1. Methodological characteristics and results of the experimental studies on memory consolidation during sleep in patients with chronic sleep disorders.

Abbreviations: DM = declarative memory; NC = narcolepsy with cataplexy; NDM = non declarative memory; OSA = obstructive sleep apnoea; PI = primary insomnia; REM = rapid eye movement (sleep); REMD = REM density; SE = sleep efficiency; SWS = slow wave sleep; SPT = sleep period time; SFI = sleep fragmentation index; SOA= stimulus onset asynchrony; TST = total sleep time; WASO = wake after sleep onset.

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Does abnormal non-rapid eye movement sleep impair declarative memory consolidation? Disturbed thalamic functions in sleep and memory processing

a Yeshiva University: Ferkauf Graduate School of Psychology, Rousso Building, 1165 Morris Park Avenue, Bronx, NY 10461, United Statesb Department of Psychiatry and Psychotherapy, University Hospital Schleswig-Holstein, University of Kiel, GermanyReceived 10 July 2010. Revised 30 July 2011. Accepted 1 August 2011. Available online 1 September 2011.View full text Non-rapid eye movement (NREM) sleep has recently garnered support for its role in consolidating hippocampus-based declarative memories in humans. We provide a brief review of the latest research on NREM sleep activity and its association with declarative memory consolidation. Utilizing empirical findings from sleep studies on schizophrenia, Alzheimer’s disease, and fibromyalgia, we argue that a significant reduction of slow-wave sleep and sleep spindle activity contribute to the development of deficits in declarative memory consolidation along with concomitant sleep disturbances commonly experienced in the aforementioned disorders. A tentative model is introduced to describe the mediating role of the thalamocortical network in disruptions of both declarative memory consolidation and NREM sleep. The hope is to stimulate new research in further investigating the intimate link between these two very important functions.

prs.rt("abs_end");NREM sleep; Sleep spindles; Slow-wave sleep; Declarative memory consolidation; Hippocampus; Thalamocortical network; Schizophrenia; Alzheimer’s disease; Fibromyalgia syndrome

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Fig. 1. During NREM sleep, abnormal thalamocortical structures may be unable to generate sufficient slow oscillations to drive the reactivation of hippocampal memory traces. These same structures may also be unable to facilitate normal spindle activity, preventing efficient declarative memory consolidation due to an absence in cortical plastic changes. Decreases in spindle activity lead to failure in inhibiting sensory information from reaching the neocortex. Thus, the individual is awakened and kept awake by sensory information, consequently experiencing disturbed NREM sleep.

View Within ArticleCopyright © 2011 Elsevier Ltd. All rights reserved.

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Does abnormal non-rapid eye movement sleep impair declarative memory consolidation? Disturbed thalamic functions in sleep and memory processing

a Yeshiva University: Ferkauf Graduate School of Psychology, Rousso Building, 1165 Morris Park Avenue, Bronx, NY 10461, United Statesb Department of Psychiatry and Psychotherapy, University Hospital Schleswig-Holstein, University of Kiel, GermanyReceived 10 July 2010. Revised 30 July 2011. Accepted 1 August 2011. Available online 1 September 2011.View full text Non-rapid eye movement (NREM) sleep has recently garnered support for its role in consolidating hippocampus-based declarative memories in humans. We provide a brief review of the latest research on NREM sleep activity and its association with declarative memory consolidation. Utilizing empirical findings from sleep studies on schizophrenia, Alzheimer’s disease, and fibromyalgia, we argue that a significant reduction of slow-wave sleep and sleep spindle activity contribute to the development of deficits in declarative memory consolidation along with concomitant sleep disturbances commonly experienced in the aforementioned disorders. A tentative model is introduced to describe the mediating role of the thalamocortical network in disruptions of both declarative memory consolidation and NREM sleep. The hope is to stimulate new research in further investigating the intimate link between these two very important functions.

prs.rt("abs_end");NREM sleep; Sleep spindles; Slow-wave sleep; Declarative memory consolidation; Hippocampus; Thalamocortical network; Schizophrenia; Alzheimer’s disease; Fibromyalgia syndrome

Figures and tables from this article:

Fig. 1. During NREM sleep, abnormal thalamocortical structures may be unable to generate sufficient slow oscillations to drive the reactivation of hippocampal memory traces. These same structures may also be unable to facilitate normal spindle activity, preventing efficient declarative memory consolidation due to an absence in cortical plastic changes. Decreases in spindle activity lead to failure in inhibiting sensory information from reaching the neocortex. Thus, the individual is awakened and kept awake by sensory information, consequently experiencing disturbed NREM sleep.

View Within ArticleCopyright © 2011 Elsevier Ltd. All rights reserved.

prs.rt('data_end');

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Does abnormal non-rapid eye movement sleep impair declarative memory consolidation? Disturbed thalamic functions in sleep and memory processing

a Yeshiva University: Ferkauf Graduate School of Psychology, Rousso Building, 1165 Morris Park Avenue, Bronx, NY 10461, United Statesb Department of Psychiatry and Psychotherapy, University Hospital Schleswig-Holstein, University of Kiel, GermanyReceived 10 July 2010. Revised 30 July 2011. Accepted 1 August 2011. Available online 1 September 2011.View full text Non-rapid eye movement (NREM) sleep has recently garnered support for its role in consolidating hippocampus-based declarative memories in humans. We provide a brief review of the latest research on NREM sleep activity and its association with declarative memory consolidation. Utilizing empirical findings from sleep studies on schizophrenia, Alzheimer’s disease, and fibromyalgia, we argue that a significant reduction of slow-wave sleep and sleep spindle activity contribute to the development of deficits in declarative memory consolidation along with concomitant sleep disturbances commonly experienced in the aforementioned disorders. A tentative model is introduced to describe the mediating role of the thalamocortical network in disruptions of both declarative memory consolidation and NREM sleep. The hope is to stimulate new research in further investigating the intimate link between these two very important functions.

prs.rt("abs_end");NREM sleep; Sleep spindles; Slow-wave sleep; Declarative memory consolidation; Hippocampus; Thalamocortical network; Schizophrenia; Alzheimer’s disease; Fibromyalgia syndrome

Figures and tables from this article:

Fig. 1. During NREM sleep, abnormal thalamocortical structures may be unable to generate sufficient slow oscillations to drive the reactivation of hippocampal memory traces. These same structures may also be unable to facilitate normal spindle activity, preventing efficient declarative memory consolidation due to an absence in cortical plastic changes. Decreases in spindle activity lead to failure in inhibiting sensory information from reaching the neocortex. Thus, the individual is awakened and kept awake by sensory information, consequently experiencing disturbed NREM sleep.

View Within ArticleCopyright © 2011 Elsevier Ltd. All rights reserved.

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Memory leak-clinical focus on practical Neurology

These are excerpts from a review in the Medical Journal of Australia (MJA):

Elderly with mild cognitive impairment are at increased risk of progression to dementia but no test is useful in evaluating this risk. Medications are not favorable in mild cognitive impairment.

Physical activity and treatment of high blood pressure decrease the risk of dementia.

In people with Alzheimer's disease, a cholinesterase inhibitor or Memantine (a receptor antagonist, N-methyl-D-aspartate) provides a symptomatic relief. Drugs do not change the progression of the disease.

Psychological and behavioral symptoms are common in Alzheimer's disease.

Atypical antipsychotics reduce agitation and psychosis, but increase the risk of cardiovascular events.

Role in the management of depression antidepressant with mild cognitive impairment is uncertain, but they may increase the risk of falls and delirium.

References:

Memory loss. Leon A Flicker, Andrew H Ford, Christopher D beer and Osvaldo p. Almeida Med J Aust 2012; 196 (2): 114-117.

Image source: hippocampus, from Wikipedia, in the public domain.

View the original article here

Read More

Memory leak-clinical focus on practical Neurology

These are excerpts from a review in the Medical Journal of Australia (MJA):

Elderly with mild cognitive impairment are at increased risk of progression to dementia but no test is useful in evaluating this risk. Medications are not favorable in mild cognitive impairment.

Physical activity and treatment of high blood pressure decrease the risk of dementia.

In people with Alzheimer's disease, a cholinesterase inhibitor or Memantine (a receptor antagonist, N-methyl-D-aspartate) provides a symptomatic relief. Drugs do not change the progression of the disease.

Psychological and behavioral symptoms are common in Alzheimer's disease.

Atypical antipsychotics reduce agitation and psychosis, but increase the risk of cardiovascular events.

Role in the management of depression antidepressant with mild cognitive impairment is uncertain, but they may increase the risk of falls and delirium.

References:

Memory loss. Leon A Flicker, Andrew H Ford, Christopher D beer and Osvaldo p. Almeida Med J Aust 2012; 196 (2): 114-117.

Image source: hippocampus, from Wikipedia, in the public domain.

View the original article here

Read More

Memory leak-clinical focus on practical Neurology

These are excerpts from a review in the Medical Journal of Australia (MJA):

Elderly with mild cognitive impairment are at increased risk of progression to dementia but no test is useful in evaluating this risk. Medications are not favorable in mild cognitive impairment.

Physical activity and treatment of high blood pressure decrease the risk of dementia.

In people with Alzheimer's disease, a cholinesterase inhibitor or Memantine (a receptor antagonist, N-methyl-D-aspartate) provides a symptomatic relief. Drugs do not change the progression of the disease.

Psychological and behavioral symptoms are common in Alzheimer's disease.

Atypical antipsychotics reduce agitation and psychosis, but increase the risk of cardiovascular events.

Role in the management of depression antidepressant with mild cognitive impairment is uncertain, but they may increase the risk of falls and delirium.

References:

Memory loss. Leon A Flicker, Andrew H Ford, Christopher D beer and Osvaldo p. Almeida Med J Aust 2012; 196 (2): 114-117.

Image source: hippocampus, from Wikipedia, in the public domain.

View the original article here

Read More