Showing posts with label Alzheimer. Show all posts
Showing posts with label Alzheimer. Show all posts

Wednesday, June 27, 2018

Donepezil for people with dementia due to Alzheimer's disease

Cochrane: What effects (benefits or harms) does donepezil have on people with dementia due to Alzheimer's disease? Alzheimer's disease is the most common cause of dementia. As the disease progresses, people lose the ability to remember, communicate, think clearly and perform the activities of daily living. Their behaviour may also change. In severe Alzheimer's disease people lose the ability to care for themselves.

Researchers discover a molecular link between post-traumatic stress disorder and Alzheimer’s disease

Heidelberg: There is increasing evidence that post-traumatic stress disorder (PTSD) increases the risk of developing dementia later in life. Researchers at the University Medical Center Göttingen, Germany, now shed light on the molecular mechanism that links the two disorders. The research is published today in The EMBO Journal.  PTSD is a brain disorder that can occur after experiencing a traumatic event. Individuals with PTSD frequently relive the traumatic event, often triggered by stimuli similar to those that accompanied the trauma. A number of epidemiological studies have shown that individuals suffering from PTSD are more prone to acquiring Alzheimer’s disease later in their lives. 

A new blood test useful to detect people at risk of developing Alzheimer’s disease

Heidelberg: There is as yet no cure for Alzheimer’s disease. It is often argued that progress in drug research has been hampered by the fact that the disease can only be diagnosed when it is too late for an effective intervention. Alzheimer’s disease is thought to begin long before patients show typical symptoms like memory loss. Scientists have now developed a blood test for Alzheimer’s disease and found that it can detect early indicators of the disease long before the first symptoms appear in patients. The blood test would thus offer an opportunity to identify those at risk and may thereby open the door to new avenues in drug discovery. The research is published today in EMBO Molecular Medicine.

Tuesday, June 12, 2018

Brain cholesterol associated with increased risk of Alzheimer’s disease

Cambridge: Researchers have shown how cholesterol – a molecule normally linked with cardiovascular diseases – may also play an important role in the onset and progression of Alzheimer’s disease. 
"The question for us now is not how to eliminate cholesterol from the brain, but about how to control cholesterol’s role in Alzheimer’s disease through the regulation of its interaction with amyloid-beta". Michele Vendruscolo

Friday, May 18, 2018

Blood test indicates risk of developing Alzheimer’s disease

DKFZ: A newly developed blood test may indicate Alzheimer's disease on average eight years before the clinical diagnosis. This was demonstrated by scientists from the Ruhr University Bochum (RUB), the German Cancer Research Center (DKFZ) and the Saarland Cancer Registry with a large population-based cohort study from the Saarland. There is as yet no cure for Alzheimer's disease. It is often argued that progress in drug research has been hampered by the fact that the disease can only be diagnosed when it is too late for an effective intervention. Alzheimer's disease is thought to begin long before patients show typical symptoms like memory loss. Scientists have now developed a blood test for Alzheimer's disease and found that it can detect early indicators of the disease long before the first symptoms appear in patients. The blood test would thus offer an opportunity to identify those at risk and may thereby open the door to new avenues in drug discovery.

Monday, May 7, 2018

Lack of sleep may be linked to risk factor for Alzheimer’s disease

NIH: Losing just one night of sleep led to an immediate increase in beta-amyloid, a protein in the brain associated with Alzheimer’s disease, according to a small, new study by researchers at the National Institutes of Health. In Alzheimer’s disease, beta-amyloid proteins clump together to form amyloid plaques, a hallmark of the disease.While acute sleep deprivation is known to elevate brain beta-amyloid levels in mice, less is known about the impact of sleep deprivation on beta-amyloid accumulation in the human brain. The study is among the first to demonstrate that sleep may play an important role in human beta-amyloid clearance.

Thursday, May 3, 2018

Concussions may increase Alzheimer's risk

SouthWestern: A new study from UT Southwestern’s Peter O’Donnell Jr. Brain Institute reveals concussions and other traumatic brain injuries may boost the risk for Alzheimer’s disease earlier in life.
Munro Cullum, Ph.D.: There’s a lot that’s still not known about concussion, it’s maximum treatment and who may be at risk for disorders later in life.

Wednesday, May 2, 2018

Antibody removes Alzheimer’s plaques, in mice

Washington University: Years before people start showing characteristic symptoms of Alzheimer’s disease, sticky plaques begin forming in their brains, damaging nearby cells. For decades, doctors have sought ways to clear out these plaques as a way to prevent or treat the disease. The sticky clumps, known as amyloid plaques, are composed primarily of a brain protein called amyloid beta. But nestled within the plaques are small amounts of another Alzheimer’s protein: APOE. Now, researchers at Washington University School of Medicine have shown that an antibody not only targets APOE for removal but sweeps away plaques.

Saturday, April 28, 2018

Uncovering the molecular mechanism behind a rare genetic risk factor of Alzheimer’s disease points to a new therapeutic target

EMBO: A gene called triggering receptor expressed on myeloid cells 2, or TREM2, has been associated with numerous neurodegenerative diseases, such as Alzheimer's disease, Frontotemporal lobar degeneration, Parkinson's disease, and Nasu-Hakola disease. Recently, a rare mutation in the gene has been shown to increase the risk for developing Alzheimer’s disease. Independently from each other, two research groups have now revealed the molecular mechanism behind this mutation. Their research, published today in EMBO Molecular Medicine, sheds light on the role of TREM2 in normal brain function and suggests a new therapeutic target in Alzheimer's disease treatment.

Researchers discover a molecular link between post-traumatic stress disorder and Alzheimer’s disease

EMBO: There is increasing evidence that post-traumatic stress disorder (PTSD) increases the risk of developing dementia later in life. Researchers at the University Medical Center Göttingen, Germany, now shed light on the molecular mechanism that links the two disorders. The research is published today in The EMBO Journal.

A new blood test useful to detect people at risk of developing Alzheimer’s disease

EMBO: There is as yet no cure for Alzheimer’s disease. It is often argued that progress in drug research has been hampered by the fact that the disease can only be diagnosed when it is too late for an effective intervention. Alzheimer’s disease is thought to begin long before patients show typical symptoms like memory loss. Scientists have now developed a blood test for Alzheimer’s disease and found that it can detect early indicators of the disease long before the first symptoms appear in patients. The blood test would thus offer an opportunity to identify those at risk and may thereby open the door to new avenues in drug discovery. The research is published today in EMBO Molecular Medicine.

Wednesday, March 8, 2017

Air pollution may lead to dementia in older women

USC: Tiny particles that pollute the air — the kind that come mainly from power plants and automobiles — may greatly increase the chance of dementia, including dementia caused by Alzheimer’s disease, according to USC-led research. Scientists and engineers found that older women who live in places with fine particulate matter exceeding the U.S. Environmental Protection Agency’s standard are 81 percent more at risk for global cognitive decline and 92 percent more likely to develop dementia, including Alzheimer’s.

Thursday, March 2, 2017

Autoimmune disease may be linked to heightened dementia risk

BMJ: Autoimmune disease may be linked to a heightened risk of dementia, indicates a large long term study, published in the Journal of Epidemiology & Community Health. Although significant, the extent of the association found was small, caution the researchers. But the findings are consistent with the theory that Alzheimer’s disease may have an autoimmune component, they point out. It has been suggested that autoimmune and inflammatory activity may have a role in the development of dementia. In a bid to try and quantify this further, the researchers drew on hospital admissions data, including day cases, from 1998 to 2012 for England.

Tuesday, February 28, 2017

New ideas on cell recycling may shape treatment of Alzheimer’s disease

SAHMRI: The secret to treating Alzheimer’s diseases may lie within the lysosome, according to researchers from the South Australian Health and Medical Research Institute. The research team, led by Dr Tim Sargeant, is exploring how the lysosomal network interacts with late-onset neurodegenerative conditions, such as Alzheimer’s disease. Dr Sargeant explained that his team is establishing a program of research that examines lysosomal function, using a range of different models. “The lysosome is the recycling centre of the cell and is critically important for long-lived, terminally-differentiated neurons (nerve cells).

Sunday, February 19, 2017

Cell disposal faults could contribute to Parkinson's, study finds

Nottingham: A fault with the natural waste disposal system that helps to keep our brain cell ‘batteries’ healthy may contribute to neurodegenerative disease, a new study has found. The research, led by academics at The University of Nottingham and published in the journal Cell Death and Disease, centres on problems with mitochondria – the powerhouses which produce energy within a cell. The results support previous evidence that patients with Parkinson’s Disease have faults with brain mitochondria which contributes to dysfunction and death within their neurons.

Saturday, February 18, 2017

Gut bacteria may play a role in Alzheimer’s disease

Lund: New research from Lund University in Sweden has shown that intestinal bacteria can accelerate the development of Alzheimer’s disease. According to the researchers behind the study, the results open up the door to new opportunities for preventing and treating the disease. Because our gut bacteria have a major impact on how we feel through the interaction between the immune system, the intestinal mucosa and our diet, the composition of the gut microbiota is of great interest to research on diseases such as Alzheimer’s. Exactly how our gut microbiota composition is composed depends on which bacteria we receive at birth, our genes and our diet.

Wednesday, February 15, 2017

Drug compound halts Alzheimer’s-related damage in mice

Saint-Louis: Under ordinary circumstances, the protein tau contributes to the normal, healthy functioning of brain neurons. In some people, though, it collects into toxic tangles that damage brain cells. Such tangles are a hallmark of Alzheimer’s and other neurodegenerative diseases. But researchers at Washington University School of Medicine in St. Louis have shown that levels of the tau protein can be reduced – and some of the neurological damage caused by tau even reversed ­– by a synthetic molecule that targets the genetic instructions for building tau before the protein is made.

Thursday, January 26, 2017

Potential of an immunotherapy demonstrated in the treatment of Alzheimer’s disease

INSERM: The involvement of the immune system in neurological diseases suggests that immunotherapy, which has shown its effectiveness in the area of cancer and autoimmune diseases, is also of major interest in the treatment of neurodegenerative diseases. This has been shown by the teams of Nathalie Cartier-Lacave (Inserm Research Director, Inserm/CEA Joint Research Unit 1169, “Gene Therapy, Genetics and Epigenetics in Neurology, Endocrinology, Cardiology and Child Development”) and David Klatzmann (Director of Inserm/Pierre and Marie Curie University Joint Research Unit 959, “Immunology – Immunopathology – Immunotherapy,” and head of the biotherapy department at Pitié-Salpêtrière Hospital, AP-HP), whose work is published today in the journal Brain. The researchers have proven that a molecule called interleukin-2 (IL-2), from the immune system, is able to control inflammation in the brain cells, which is implicated in neurodegenerative diseases such as Alzheimer’s disease, and can restore impaired cognitive functions in the animal model.

Saturday, January 14, 2017

Evidence of Alzheimer's in Patients with Lewy Body Disease Tracks with Course of Dementia

Philadelphia: Patients who had a diagnosis of Parkinson’s disease (PD) with dementia (PDD) or dementia with Lewy bodies (DLB) and had higher levels  of Alzheimer’s disease (AD) pathology in their donated post-mortem brains also had more severe symptoms of these Lewy body diseases (LBD) during their lives, compared to those whose brains had less AD pathology, according to research from the Perelman School of Medicine at the University of Pennsylvania. In particular, the degree of abnormal tau protein aggregations, indicative of AD, most strongly matched the clinical course of the LBD patients who showed evidence of dementia prior to their deaths, the team reports in The Lancet Neurology First Online, ahead of the January print edition.

Friday, January 6, 2017

Alzheimer’s disease: deleterious effects from the immune system?

ICM: Alzheimer’s disease is a neurodegenerative disease characterized by two types of lesions: amyloid lesions and neurofibrillary tangles linked with the accumulation of aggregated Tau proteins. As part of a collaborative project between the Centre de Recherche Jean-Pierre Aubert (Inserm UMR-S 1172, Université de Lille), the ICM and the Centre de Recherche St Antoine, researchers looked at the activation of the immune system in a mouse model of Tauopathy, mimicking the degeneration caused by the Tau protein. They showed an infiltration of pathogenic T-cells in the animals’ brain, with deleterious effects on cognitive functions. Their results, published in Brain, open the way to the identification of novel therapeutic targets to treat the disease.