Tag Archives: Hippocampus

Sleep deprivation associated with changes in brain micro-structure

9 Oct

A paper from PLOS , “Widespread Changes in White Matter Microstructure after a Day of Waking and Sleep Deprivation.”

From the PLOS Blog:

“Neuroscientists from Norway set out to answer this question in their recent PLOS ONE study, examining how a night forgoing sleep affects brain microstructure. Among their findings, sleep deprivation induced widespread structural alterations throughout the brain.”

“My hypothesis,” says first author Dr. Torbjørn Elvsåshagen, “would be that the putative effects of one night of sleep deprivation on white matter microstructure are short term and reverse after one to a few nights of normal sleep. However, it could be hypothesized that chronic sleep insufficiency might lead to longer-lasting alterations in brain structure. Consistent with this idea, evidence for an association between impaired sleep and localized cortical thinning was found in obstructive sleep apnea syndrome, idiopathic rapid eye movement sleep behavior disorder, mild cognitive impairment and community-dwelling adults. Whether chronic sleep insufficiency can lead to longer-lasting alterations in white matter structure remains to be clarified.”

Treadmill Running Reverses Cognitive Declines

5 Feb

A paper from Medicine & Science in Sports & Exercise:

“Purpose: This study investigated the effect of treadmill running on cognitive declines in the early and advanced stages of Alzheimer’s disease (AD) in 3xTg-AD mice.

Methods: At 4 months of age, 3xTg-AD mice (N=24) were assigned to control (AD+CON, n=12) or exercise (AD+EX, n=12) group. At 24 months of age, 3xTg-AD mice (N=16) were assigned to AD+CON (n=8) or AD+EX (n=8) group. The AD+EX mice were subjected to treadmill running for 12-week. At each pathologic stage, the background strain mice were included as wild type control (WT+CON, n=8-12).

Results: At the early stage of AD, 3xTg-AD mice had impaired short- and long-term memory based on Morris water maze along with higher cortical A[beta] deposition, higher hippocampal and cortical tau pathology, and lower hippocampal and cortical PSD-95 and synaptophysin. A 12-week treadmill running reversed the impaired cognitive declines and significantly improved the tau pathology along with suppression of the decreased PSD-95 and synaptophysin in the hippocampus and cortex. At the advanced stage of AD, 3xTg-AD mice had impaired short- and long-term memory along with higher levels of A[beta] deposition, soluble A[beta]1-40 and A[beta]1-42, tau pathology, and lower levels of BDNF, PSD-95 and synaptophysin in the hippocampus and cortex. A 12-week treadmill running reversed the impaired cognitive declines and significantly improved the A[beta] and tau pathology along with suppression of the decreased synaptic proteins and BDNF in the hippocampus and cortex.

Conclusion: The current findings suggest that treadmill running provides a non-pharmacologic means to combat cognitive declines due to AD pathology.”

 

 

Transcranial magnetic Stimulation, improves memory. Maybe.

3 Sep

A recent paper, in the prestigious journal Science, reports that transcranial magnetic stimulation may improve memory. Unfortunately, the article is behind a pay wall so I am unable to present a critical analysis. Here is the abstract:

“The influential notion that the hippocampus supports associative memory by interacting with functionally distinct and distributed brain regions has not been directly tested in humans. We therefore used targeted noninvasive electromagnetic stimulation to modulate human cortical-hippocampal networks and tested effects of this manipulation on memory. Multiple-session stimulation increased functional connectivity among distributed cortical-hippocampal network regions and concomitantly improved associative memory performance. These alterations involved localized long-term plasticity because increases were highly selective to the targeted brain regions, and enhancements of connectivity and associative memory persisted for ~24 hours after stimulation. Targeted cortical-hippocampal networks can thus be enhanced noninvasively, demonstrating their role in associative memory.”

From Science Daily here is a journalistic account of the research:

“Stimulating a region in the brain via non-invasive delivery of electrical current using magnetic pulses, called Transcranial Magnetic Stimulation, improves memory. The discovery opens a new field of possibilities for treating memory impairments caused by conditions such as stroke, early-stage Alzheimer’s disease, traumatic brain injury, cardiac arrest and the memory problems that occur in healthy aging.”

However, there has been some criticism of these findings (hat tip to Retraction Watch)

 

Electric Current to Brain Boosts Memory from Northwestern News on Vimeo.

More good news on exercise and Alzheimer’s

4 Jul

From The New York Times, “Can Exercise Reduce Alzheimer’s Risk?”

“Exercise may help to keep the brain robust in people who have an increased risk of developing Alzheimer’s disease, according to an inspiring new study. The findings suggests that even moderate amounts of physical activity may help to slow the progression of one of the most dreaded diseases of aging.”

You can read the original paper here. Here is the abstract:

“We examined the impact of physical activity (PA) on longitudinal change in hippocampal volume in cognitively intact older adults at varying genetic risk for the sporadic form of Alzheimer’s disease (AD). Hippocampal volume was measured from structural magnetic resonance imaging (MRI) scans administered at baseline and at an 18-month follow-up in 97 healthy, cognitively intact older adults. Participants were classified as High or Low PA based on a self-report questionnaire of frequency and intensity of exercise. Risk status was defined by the presence or absence of the apolipoprotein E-epsilon 4 (APOE-ε4) allele. Four subgroups were studied: Low Risk/High PA (n = 24), Low Risk/Low PA (n = 34), High Risk/High PA (n = 22), and High Risk/Low PA (n = 17). Over the 18 month follow-up interval, hippocampal volume decreased by 3% in the High Risk/Low PA group, but remained stable in the three remaining groups. No main effects or interactions between genetic risk and PA were observed in control brain regions, including the caudate, amygdala, thalamus, pre-central gyrus, caudal middle frontal gyrus, cortical white matter (WM), and total gray matter (GM). These findings suggest that PA may help to preserve hippocampal volume in individuals at increased genetic risk for AD. The protective effects of PA on hippocampal atrophy were not observed in individuals at low risk for AD. These data suggest that individuals at genetic risk for AD should be targeted for increased levels of PA as a means of reducing atrophy in a brain region critical for the formation of episodic memories.”

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