links on 40hz therapy
LISTENING to low-pitched noise seems to induce high-speed brainwaves that break down protein plaques in the brain linked with Alzheimer’s. The approach has had promising results in mice and is now being tested in people with the condition.
Brainwaves are the result of large networks of brain cells firing rhythmically and in synchrony. Much about their function is unclear, but measuring these waves via electrodes on the scalp tells us that their frequency tends to reflect how awake and alert we feel.
Brainwaves are slowest during deep sleep, and faster when we’re awake and relaxed. …
Brain-Wave Treatment for Alzheimer’s Is Promising, but the First Human Subject Is Left Behind
and
December 08, 2017
Peg Gleason, who is 83 and lives in San Francisco, was the first to sign up for the initial human trial of an MIT-backed experimental treatment for Alzheimer’s disease last January.
The trial had a slightly eccentric setting at the warehouse offices of TheraNova, a San Francisco-based medical-device developer. Seven days a week for seven months, until the study ended,
Short-Term Effects of Rhythmic Sensory Stimulation in Alzheimer’s Disease: An Exploratory Pilot Study
Amy Clements-Cortes 1 2 3 4 , Heidi Ahonen 2 , Michael Evans 3 , Morris Freedman 4 , Lee Bartel 1
Affiliations
- PMID: 27031491
- DOI: 10.3233/JAD-160081
Abstract
This study assessed the effect of stimulating the somatosensory system of Alzheimer’s disease (AD) patients at three stages of their illness with 40 Hz sound. In this AB cross-over study design, 18 participants (6 mild, 6 moderate, 6 severe) each participated in 13 sessions: one intake and 12 treatment. Treatment A consisted of 40 Hz sound stimulation and Treatment B consisted of visual stimulation using DVDs, each provided twice a week over 6 weeks for a total of 6 times per treatment. Outcome measures included: St. Louis University Mental Status Test (SLUMS), Observed Emotion Rating Scale, and behavioral observation by the researcher. Data were submitted to regression analysis for the series of 6 SLUMS scores in treatment A and 6 scores in B with comparison by group. The slopes for the full sample and subgroups in the 40 Hz treatment were all significant beyond alpha = 0.05, while those for the DVD were not. A thematic analysis of qualitative observations supported the statistical findings. 40 Hz treatment appeared to have the strongest impact on persons with mild and moderate AD. Results are promising in terms of a potential new treatment for persons with AD, and further research is needed.
*NOTE: This research has made major new strides since 2016. For a more up-to-date version, please see http://www.youtube.com/watch?v=2W4ZdX…. Researchers in Li-Huei Tsai’s laboratory at the Picower Institute for Learning and Memory have shown that disrupted gamma waves in the brains of mice with Alzheimer’s disease can be corrected by a unique non-invasive technique using flickering light. (Learn more: http://news.mit.edu/2016/visual-stimu…)
Beating Alzheimer’s With Brain Waves
In a completely new approach, scientists reduced a hallmark of the disease in mice by stimulating their neurons with flickering lights.
Abstract
Changes in gamma oscillations (20-50 Hz) have been observed in several neurological disorders. However, the relationship between gamma and cellular pathologies is unclear. Here, we show reduced behaviorally-driven gamma before the onset of plaque formation or cognitive decline in a mouse model of Alzheimer’s disease (AD). Optogenetically driving FS-PV-interneurons at gamma (40 Hz), but not other frequencies, reduced levels of amyloid-β (A β)1-40 and A β1-42 isoforms. Gene expression profiling revealed induction of genes associated with morphological transformation of microglia and histological analysis confirmed increased microglia co-localization with A β. Subsequently, we designed a non-invasive 40 Hz light-flickering paradigm that reduced A β1-40 and A β1-42 levels in visual cortex of pre-depositing mice and mitigated plaque load in aged, depositing mice. Our findings uncover a previously unappreciated function of gamma rhythms in recruiting both neuronal and glial responses to attenuate AD-associated pathology.
Activation of local circuits of excitatory and fast-spiking inhibitory neurons that resonate at 20-50 Hz gives rise to oscillations in the local field potential (LFP), called gamma oscillations.1–3 Although studies have demonstrated disrupted gamma in various neurological diseases, the interplay between pathology and this emergent circuit property has yet to be determined.4,5 In general, molecular and cellular pathology is thought to alter synaptic activity. However, in at least one disorder, Alzheimer’s disease (AD), changes in synaptic activity can also feedback to alter molecular pathology. Studies have shown that increases in synaptic activity in vivo increase levels of amyloid-β (A β),6 a 36-43 amino acid protein, whose aggregation is thought to initiate neurotoxic events, including neuroinflammation, synaptic and neuronal
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