Commenting on the study for Medscape Medical News, Heather Snyder, PhD, director, medical and scientific relations, Alzheimer’s Association, Chicago, Illinois, said a number of studies have shown that lifestyle interventions can attenuate the progressive decline in cognitive function in older individuals.
Most recently, the FINGER study (Finnish Geriatric Intervention Study to Prevent Cognitive Impairment and Disability), which was presented earlier this year at the Alzheimer’s Association International Conference 2014 and was reported by Medscape Medical News at that time, showed that a multipronged lifestyle intervention had a significant beneficial effect on overall cognitive performance, including memory, executive function, and psychomotor speed, in a large cohort of older participants at high risk for cognitive decline.
“The FINGER study certainly suggests that this is the kind of study we need to do in translating what Dr Bredesen did to a much larger clinical trial,” Dr Snyder said.
Dr Snyder also noted that it is clear the underlying pathology driving AD is already changing well before patients manifest overt memory loss
The interventions used in the 10 patients involved in the UCLA pilot project were tailored to each individual, but they shared similar elements. Typically, patients were asked to eliminate all simple carbohydrates from their diet.
They were also asked to increase consumption of fruit, vegetables, and nonfarmed fish and to follow a strict meal pattern with specifically timed interludes of fasting.
Exercise was a key component of all interventions, and participants were counseled on ways to reduce stress through practices such as yoga and meditation.
Participants also took a large variety of daily supplements, including vitamin D3, fish oil, coenzyme Q10, melatonin, and methylcobalamin.
And where appropriate, practitioners counseled their female patients to resume previously discontinued hormone replacement therapy.
“The program is not easy to follow,” Dr Bredesen acknowledged. (None of the patients in this pilot project were able to fully follow the program).
“But what this program says is that we are all contributing to our own AD by the diet we chose to eat; by the way we sleep; by the stress we hav
In studies of transgenic mice, Dr Bredesen and colleagues found that beta-amyloid precursor protein (APP) signaling can be manipulated to inhibit the underlying pathophysiology that causes AD.
However, many different metabolic factors contribute to APP signaling, including hormones, inflammatory mediators, and exercise.
This suggests that the pathobiology of AD must be approached at different points of intervention and not with a single targeted agent.
“Just as for other chronic illnesses such as atherosclerotic cardiovascular disease, the goal is not simply to normalize metabolic parameters, but rather to optimize them,” the investigators write.
“Based on the hypothesis that AD results from an imbalance in an extensive plasticity network, the therapy should address as many network components as possible, with the idea that a combination approach may create an effect that is more than the sum of the effects of many monotherapeutics,” the researchers add.
Critical to the success of this hypothesis is the idea that there is a “threshold” at which multiple interventions will start to reverse the pathology leading to memory loss.
A total of 10 patients with memory loss associated with either AD, mild cognitive impairment, or subjective cognitive impairment were recruited for the study.
Each participant was instructed to follow a personalized intervention program tailored to address specific metabolic deficits identified on laboratory testing as affecting the plasticity of the participant’s brain, causing memory loss.
Nine of the 10 patients displayed subjective or objective improvement in cognition within 3 to 6 months of initiation of treatment. The single patient who failed to respond to the intervention had late-stage AD.
Six participants had discontinued working or were struggling with their jobs at study outset because of memory problems.
“All were able to return to work or continue working with improvement performance, and improvements have been sustained,” said Dr Bredesen.
At the present time, one patient has been followed for 2.5 years from the initial presentation, and the patient continues to show “sustained and marked improvement.”
Dr Bredesen noted that the level of improved function required to work effectively
Los pacientes con migraña crónica (MC) y abuso de medicación son difíciles de tratar y tienen peor calidad de vida que otros pacientes con migrañas, por lo que un estudio ha pretendido valorar si la presencia de abuso de fármacos disminuye la efectividad del topiramato.
Para ello se seleccionaron 262 pacientes con criterios de MC, y de ellos 167 (63,7%) cumplieron criterios de abuso. Se les aconsejó la supresión del fármaco del cual abusaban, se ajustó el tratamiento de sus crisis y se inició tratamiento preventivo desde el principio con topiramato. Luego se valoró el número días con cefalea y migrañas intensas en el mes previo y al cuarto mes de tratamiento. En ambos grupos (abuso o no abuso de fármacos) hubo un porcentaje de reducción significativo del número de días con cefalea/mes al cuarto mes de tratamiento con topiramato: 59,3 ± 36,1% en el grupo sin abuso y 48,7 ± 41,7% en el grupo con abuso (p = 0,0574). Respecto al porcentaje de reducción de migrañas intensas/mes: 61,2% en el grupo sin abuso y 50% en el grupo con abuso de fármacos (p = 0,0224).
Los autores concluyen que el topiramato fue efectivo en pacientes con MC sin y con abuso de fármacos, aunque con menor efectividad en estos últimos.
Los niños con antecedentes de prematuridad presentan mayor frecuencia de problemas graves en el neurodesarrollo y de problemas cognitivos, entre los que destacan las funciones visuoespaciales. Un estudio ha revisado qué factores están implicados en el desarrollo de estas funciones y qué circunstancias pueden interferir en su buen desarrollo.
Diferentes estudios muestran que los niños prematuros o con bajo peso al nacer obtienen menores puntuaciones en los tests que valoran las funciones cognitivas, siendo estas diferencias más pronunciadas durante el primer año de vida. Con el tiempo, estas diferencias se van atenuando, pero persiste un retraso madurativo que afecta a la memoria de trabajo y a los procesos visuoespaciales. Al respecto, se han descrito diferencias anatómicas y fisiológicas entre el cerebro del niño pretérmino y el término que podrían explicar, en parte, alguna de estas alteraciones.
La lesión de la sustancia blanca típica del cerebro inmaduro se ha postulado como la responsable de esta disfunción cognitiva y del anormal desarrollo de la sustancia gris, siendo la leucomalacia periventricular la causa de las alteraciones atencionales y visuoespaciales del niño prematuro debido a la vulnerabilidad de las regiones que intervienen en la
Long-term use of both mobile and cordless phones is associated with an increased risk for glioma, the most common type of brain tumor, the latest research on the subject concludes.
The new study shows that the risk for glioma was tripled among those using a wireless phone for more than 25 years and that the risk was also greater for those who had started using mobile or cordless phones before age 20 years.
“Doctors should be very concerned by this and discuss precautions with their patients,” study author Lennart Hardell, MD, PhD, professor, Department of Oncology, University Hospital, Örebro, Sweden, told Medscape Medical News.
Such precautions, he said, include using hands-free phones with the “loud speaker” feature and text messaging instead of phoning.
The study was published online October 28 in Pathophysiology.
The recent worldwide increase in use of wireless communications has resulted in greater exposure to radiofrequency electromagnetic fields (RF-EMF). The brain is the main ta
A novel, comprehensive lifestyle intervention has shown promise in reversing memory loss related to Alzheimer’s disease (AD), preliminary research suggests.
According to investigators, this novel intervention is aimed at “tweaking” the network of imbalances in the brain that contribute to cognitive decline.
“We’ve been studying the underlying mechanisms of neurodegeneration in the test tube and in transgenic mice for 25 years, and we came to the conclusion that there is an imbalance between the physiological processes that mediate plasticity in Alzheimer’s disease ― between synaptoblastic and synaptoclastic signaling — similar to what we see in osteoporosis, where osteoblastic signaling is chronically exceeded by osteoclastic signaling, resulting in bone loss,” principal investigator Dale Bredesen, MD, professor of neurology and director, Mary S. Easton Center for Alzheimer’s Disease Research, University of California, Los Angeles, told Medscape Medical News.
Through this lifestyle intervention, “it appears we can correct this network imbalance by tweaking it at multiple sites,” Dr Bredesen added.
The study was