Scientists found that when mice engineered to exhibit Alzheimer’s-like qualities were exposed to flickering lights and 40Hz sounds for one hour a day, their brain functions improved and toxic levels of Alzheimer’s-related proteins diminished. In addition, the 40Hz sound appeared to improve cognitive and memory skills.
Light and sound delivered at a certain frequency —40 flashes or clicks per second — appear to restart the natural 40Hz gamma rhythm of the brain, which is disrupted in patients with Alzheimer’s. This gamma rhythm is essential for local neuronal communication and is associated with concentration and cognitive activity. Neurons in the cortex usually work in groups and are a bit analogous to a musical orchestra. When music instruments synchronize we hear a pleasant melody, but when they desynchronize we hear a cacophony of sounds a little like the tuning up of an orchestra. Similarly, when there is no normal brain rhythm, neurons fire out of sync and cannot generate coherent group decisions.
The improved 40Hz brain gamma waves appear to increase activation of immune cells that became more efficient at chewing up the harmful proteins that form plaques and tangles in Alzheimer’s brain. The 40Hz sound also improved brain blood vessels, further helping clear the toxic proteins. Most importantly, these combined effects of light and sound extended to the prefrontal cortex, which probably explains significant improvement of the cognitive functions.
Experiments also showed that without the light or sound stimulation, results faded in about a week, indicating that Alzheimer’s patients might need to be treated regularly.
A brain training computer game developed by British neuroscientists has been shown to improve the memory of patients in the very earliest stages of dementia and could help such patients avert some symptoms of cognitive decline.
Experimental drugs from some of the world’s top pharmaceutical companies have so far failed to halt the march of Alzheimer’s disease, a neurodegenerative disorder that gradually robs people of their memory and cognition.
Now scientists are trying an audacious approach that doesn’t involve medicines of any kind: They’re using LED beams to disrupt gamma waves in the brains of lab mice, hoping to reduce the buildup of beta amyloid plaque — a substance widely thought to contribute to Alzheimer’s.
When brain cells fire rhythmically and in sync, they produce waves, which are categorized by their firing frequencies. Delta waves (1.5 Hz to 4 Hz), for example, are produced during deep sleep, theta waves (4 Hz to 12 Hz) occur during running and deep meditation, and gamma waves (25 Hz to 100 Hz) are associated with excitement and concentration. Disruption of gamma waves could be a key contributor to Alzheimer’s disease pathology, according to a mouse study published today (December 7) in Nature. And the restoration of these waves, researchers propose, may one day be an option for Alzheimer’s disease treatment.
Changes in gamma oscillations (20–50 Hz) have been observed in several neurological disorders. However, the relationship between gamma oscillations and cellular pathologies is unclear. Here we show reduced, behaviourally driven gamma oscillations before the onset of plaque formation or cognitive decline in a mouse model of Alzheimer’s disease. Optogenetically driving fast-spiking parvalbumin-positive (FS-PV)-interneurons at gamma (40 Hz), but not other frequencies, reduces levels of amyloid-β (Aβ)1–40 and Aβ 1–42 isoforms. Gene expression profiling revealed induction of genes associated with morphological transformation of microglia, and histological analysis confirmed increased microglia co-localization with Aβ. Subsequently, we designed a non-invasive 40 Hz light-flickering regime that reduced Aβ1–40 and Aβ1–42 levels in the 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 Alzheimer’s-disease-associated pathology.
A flashing light therapy might help ward off Alzheimer’s, say US scientists after promising trials in mice.
The Massachusetts team found shining a strobe light into rodents’ eyes encouraged protective cells to gobble up the harmful proteins that accumulate in the brain in this type of dementia.
The perfect rate of flashes was 40 per second – a barely perceptible flicker, four times as fast as a disco strobe.
The researchers say the approach should be tested in humans.
They are already seeking permission from the US regulator, the Food and Drugs Administration, and have set up a commercial company to develop the technology.
Cognitive training and cognitive rehabilitation for mild to moderate Alzheimer’s disease and vascular dementiaPublished on Jan 01,2013 | By Cochrane Library
Cognitive impairments, particularly memory problems, are a defining feature of the early stages of Alzheimer’s disease (AD) and vascular dementia. Cognitive training and cognitive rehabilitation are specific interventional approaches designed to address difficulties with memory and other aspects of cognitive functioning. The present review is an update of previous versions of this review.
The main aim of the current review was to evaluate the effectiveness and impact of cognitive training and cognitive rehabilitation for people with mild Alzheimer’s disease or vascular dementia in relation to important cognitive and non-cognitive outcomes for the person with dementia and the primary caregiver in the short, medium and long term.
The present paper presents data from ten patients suffering from mild to moderate Alzheimer’s disease (AD), all of whom were trained to use an interactive computer-based program. Using photographs of the patient and his or her personal surroundings, an everyday task of relevance to the patient was simulated on a PC-touch screen, which the patient was trained to operate. After three weeks of training (three to four sessions a week), the patients needed less help in performing the programs, they became faster, and eight out of ten made fewer mistakes. The results were most pronounced in patients with a poor performance at the beginning, and there was no difference between early-onset (EO) and late-onset (LO) AD patients. Although the training was generally well received, there was no evidence of a general cognitive improvement, and it remains an open question whether the results achieved with PC training can be transferred to real-life situations.
Cognitive Training Using a Novel Memory Game on an iPad in Patients with Amnestic Mild Cognitive Impairment (aMCI)Published on Dec 01,1996 | By Oxford Academic
Significant time-by-pattern-by-group interactions were found for cognitive performance in terms of the number of errors made and trials needed on the Cambridge Neuropsychological Test Automated Battery Paired Associates Learning task (P=.044; P=.027). Significant time-by-group interactions were also found for the Cambridge Neuropsychological Test Automated Battery Paired Associates Learning first trial memory score (P=.002), Mini-Mental State Examination (P=.036), the Brief Visuospatial Memory Test (P=.032), and the Apathy Evaluation Scale (P=.026). Within-group comparisons revealed highly specific effects of cognitive training on episodic memory. The cognitive training group maintained high levels of enjoyment and motivation to continue after each hour of gameplay, with self-confidence and self-rated memory ability improving over time.
Episodic memory robustly improved in the cognitive training group. “Gamified” cognitive training may also enhance visuospatial abilities in patients with amnestic mild cognitive impairment. Gamification maximizes engagement with cognitive training by increasing motivation and could complement pharmacological treatments for amnestic mild cognitive impairment and mild Alzheimer’s disease. Larger, more controlled trials are needed to replicate and extend these findings.