Showing posts with label Mild cognitive impairment. Show all posts
Showing posts with label Mild cognitive impairment. Show all posts

Sharpening Your Synapses: Spermidine Reverses Age Related Memory Decline – Neuroscience News

In the article published September 29 in open-access journal PLOS Biology, work by the groups of Stephan Sigrist from the Freie Universität Berlin, Andrea Fiala (Universität Göttingen) and Frank Madeo (Universität Graz) now shows that specific changes at the level of synapses directly provoke age-related dementia, and that, however, administering a simple substance already found in our bodies, spermidine, can help to avoid such age-related synaptic changes and thereby protect from age-induced memory impairment.

Just like humans, the fruit fly Drosophila melanogaster – a leading model for aging research – suffers from memory impairment with advancing age. The same team of researchers previously observed that Drosophila exhibits an age-induced decline in levels of spermidine, and that these memory deficits can be suppressed by feeding with a diet supplemented by spermidine.

They now describe an unexpected scenario that convincingly explains the suppression of memory deficits by spermidine feeding. In a nutshell, synapses within the Drosophila brain seem to narrow their operational space, and thus become increasingly unable to form new memories with age.

Dietary supplementation with spermidine, however, prevented these changes. Importantly, when the authors mimicked these age-associated changes by genetic means, learning suffered even in young flies, providing a causal link between generic synaptic mechanisms and age-induced memory impairment."





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LDL phenotype in subjects with mild cognitive impairment and Alzheimer's disease.

Centenarians with normal cognitive function have a "longevity phenotype" characterized by large low-density lipoproteins (LDL) and high-density lipoproteins (HDL) and low incidence of metabolic syndrome, hypertension, and cognitive impairment. Alzheimer's disease (AD) is associated with a number of cardiovascular risk factors, but it is not known if they have or lack the "longevity phenotype".
OBJECTIVE:
The study was designed to determine LDL size and body fat content and distribution in subjects with mild cognitive impairment (MCI) and AD.
RESULTS:Fifty-eight persons with MCI or AD (cases) and 42 control subjects of similar age
had measurement of LDL size and lipoprotein lipids after a 12 h fast and analysis of body composition by dual x-ray absorptiometry. Cases had small LDL size more often than controls (73% versus 66%) associated with significantly higher triglycerides, lower HDL cholesterol, and higher
triglyceride/HDL cholesterol ratio (p ≤ 0.02). Cases with large LDL had a better lipoprotein profile than those with small LDL. Cases and controls had similar percent body fat, fat index, and lean mass index. Forty-seven percent of cases and 39% of controls were obese.

CONCLUSION:

The prevalence of small LDL phenotype in MCI and AD cases contrasts with
the "longevity phenotype" reported for centenarians with preserved
cognitive function. The small LDL phenotype is an atherogenic
lipoprotein profile found in metabolic syndrome, type 2 diabetes, and
insulin resistance. It is now also reported in persons with MCI and AD.
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Increase in the IgG avidity index due to herpes simplex virus type 1 reactivation and its relationship with cognitive function in amnestic mild cognitive impairment and Alzheimer's disease.

 After infection with herpes simplex virus type 1 (HSV-1), latent infection persists for life in the trigeminal ganglion and reactivation results in an outbreak of cold sores around the mouth. Many previous studies have reported HSV-1 reactivation to be a risk factor for Alzheimer's disease (AD). This study enrolled subjects with AD (n=85), subjects with amnestic mild cognitive impairment (aMCI; a prodromal stage of AD) (n=34), and healthy controls (n=28). The avidity index of anti-HSV-1 IgG antibodies--a known indicator of HSV-1 reactivation--was measured in order to clarify the relationship between HSV-1 reactivation and symptoms of cognitive function in AD. Cognitive function in AD and aMCI were evaluated using scores from the mini-mental state examination (MMSE) and frontal assessment battery (FAB). The results showed that the subjects with aMCI, for which cerebral function is better preserved than subjects with AD, had a higher anti-HSV-1 IgG antibody avidity index than the AD subjects or healthy controls. Furthermore, the anti-HSV-1 IgG antibody avidity index was even higher in the subjects with high MMSE scores on orientation to time and three-step command subscores. We observed a negative correlation between the anti-HSV-1 IgG antibody avidity index and plasma BDNF concentration, which is an indicator of encephalitis. This suggests that HSV-1 reactivation, as observed through an increase in the anti-HSV-1 IgG avidity index, does not progress to encephalitis. These results suggest that HSV-1 reactivation occurs from the stage of aMCI, which is prodromal to AD, and can affect AD symptoms without an intermediary stage of severe encephalitis. The study demonstrates that the anti-HSV-1 IgG antibody avidity index could be a useful biomarker for the early diagnosis of aMCI as well as AD, and suggests that antiviral medication to treat HSV-1 could play a role in preventing the onset of AD.

Inappropriate treatments for patients with cognitive decline.


Some treatments are inappropriate for patients with cognitive decline. We analyse their use in 500 patients and present a literature review.

DEVELOPMENT:

Benzodiazepines produce dependence, and reduce attention, memory, and motor ability. They can cause disinhibition or aggressive behaviour, facilitate the appearance of delirium, and increase accident and mortality rates in people older than 60. In subjects over 65, low systolic blood pressure is associated with cognitive decline. Maintaining this figure between 130 and 140mm Hg (145 in patients older than 80) is recommended. Hypocholesterolaemia<160mg/dl is associated with increased morbidity and mortality, aggressiveness, and suicide; HDL-cholesterol<40mg/dl is associated with memory loss and increased vascular and mortality risks. Old age is a predisposing factor for developing cognitive disorders or delirium when taking opioids. The risks of prescribing anticholinesterases and memantine to patients with non-Alzheimer dementia that is not associated with Parkinson disease, mild cognitive impairment, or psychiatric disorders probably outweigh the benefits. Anticholinergic drugs acting preferentially on the peripheral system can also induce cognitive side effects. Practitioners should be aware of steroid-induced dementia and steroid-induced psychosis, and know that risk of delirium increases with polypharmacy. Of 500 patients with cognitive impairment, 70.4% were on multiple medications and 42% were taking benzodiazepines. Both conditions were present in 74.3% of all suspected iatrogenic cases.

CONCLUSIONS:

Polypharmacy should be avoided, if it is not essential, especially in elderly patients and those with cognitive impairment. Benzodiazepines, opioids and anticholinergics often elicit cognitive and behavioural disorders. Moreover, systolic blood pressure must be kept above 130mm Hg, total cholesterol levels over 160mg/dl, and HDL-cholesterol over 40mg/dl in this population.
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Caffeine may block inflammation linked to mild cognitive impairment

Recent studies have linked caffeine consumption to a reduced risk of Alzheimer's disease, and a new University of Illinois study may be able to explain how this happens.

Read more at: http://medicalxpress.com/news/2012-10-caffeine-block-inflammation-linked-mild.html#jCp

High blood caffeine levels in older adults linked to avoidance of Alzheimer’s disease

This was linked to the caffeine in coffee rather than tea, and suggested that caffeine intake might be able to delay the onset of Alzheimer's disease in individuals with mild cognitive impairment.Cao et al, 2012


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