What is Alzheimer's Disease?

Scientists aren’t absolutely sure what causes cell death and tissue loss in the Alzheimer's brain, but the plaques and tangles are prime suspects.

Does Memory Loss Always Mean Dementia?

Dementia is a broad category of symptoms that affect the brain and causes memory loss.

Early onset Alzheimer's

Although, Alzheimer’s is viewed as a disease of the elderly, up to 5% of Americans with Alzheimer’s have the early-onset variety, which can start to show symptoms as early as one’s 30s.

Showing posts with label Brain. Show all posts
Showing posts with label Brain. Show all posts

Monday, September 9, 2019

Chronic Stress Damages Brain, Increases Risk of Dementia


Chronic stress

People with chronic stress and anxiety are at an increased risk of developing depression and even dementia, a new research has shown.

When the researchers noticed that mental illness is aggravated by stress, they aimed to address the question of whether anxiety damages the brain and whether they could identify mechanisms behind the connection between stress and mental illness.

For their research, the tem - led by Dr. Linda Mah of the Rotman Research Institute at Baycrest Health Sciences in Canada reviewed animal and human studies that examined brain areas affected by chronic anxiety, fear and stress that are already published. They reported finding "extensive overlap" of the brain's neurocircuitry in all three conditions, which they said may justify the link between chronic stress and the development of neuropsychiatric disorders, including depression and Alzheimer's disease.

Read more Does Memory Loss Always Mean Dementia?

Occasional and temporary fear and stress is normal part of life. This is common among people to feel stressed and anxious before a job interview or an exam. However, when these reactions become chronic or frequent, they can affect daily lives and interfere with work, school and relationships.

Chronic stress is a pathological state. It is caused by stress causing disruption on immune, metabolic and cardiovascular systems, which leads to decay of the brain's hippocampus (crucial for long-term memory and spatial navigation).

Read more Study:Access to nature makes men and seniors sleep better

Dr. Linda Mah, clinician scientist with Baycrest's Rotman Research Institute and lead author of the review said:

"Pathological anxiety and chronic stress are associated with structural degeneration and impaired functioning of the hippocampus and the prefrontal cortex (PFC), which may account for the increased risk of developing neuropsychiatric disorders, including depression and dementia.”

Read more Blueberries May Help Fight Alzheimer’s

A man with dementia

Dr. Mah and colleagues focused on key structures in the neurocircuitry of fear and anxiety – amygdala, medial prefrontal cortex, hippocampus. These brain areas are impacted during chronic stress. The researchers noted similar patterns of abnormal brain activity with fear, anxiety and chronic stress – specifically an overactive amygdala (associated with emotional responses) and an under-active PFC (thinking areas of the brain that help regulate emotional responses through cognitive appraisal).

Read more PsychiatricDisorders More Prevalent Among Workaholics

This see-saw relationship was first identified in a landmark study by world-renowned neurologist and depression researcher Dr. Helen Mayberg over a decade ago.

However, Dr. Mah also suggests that damage to the hippocampus and PFC as a result of stress can be reversible. She said that both anti-depressant treatment and physical activity have both shown promise in increasing hippocampal neurogenesis.

Read more HowArtificial Intelligence Can Predict Premature Death

The researchers conclude their study by writing:

"Whether anti-anxiety interventions can reduce risk of developing neuropsychiatric illness needs to be established with longitudinal studies."

The paper is posted online this month in the journal Current Opinion in Psychiatry.

Saturday, June 23, 2018

Alzheimer’s brain plaques found in people with traumatic brain injury


Alzheimer’s brain plaques found in people with traumatic brain injury

A new study, published in the journal Neurology suggests people with traumatic brain injury (TBI) may have buildup of plaques similar to those found in the brains of Alzheimer’s patients. Although these amyloid plaques match, their spatial distribution differs.

A corresponding editorial says that over the past decade the rate of emergency department visits related to traumatic brain injury (TBI) has increased by 70% in the United States. The editorial also says an estimated three to five million Americans live with a TBI-related disability.


TBI occurs when the brain experiences damage due to a sudden trauma.

Study author Prof. David Sharp, MD, of Imperial College London said:
"The study is small and the findings preliminary; however, we did find an increased buildup of amyloid plaques in people who had previously sustained a traumatic brain injury.”

"The areas of the brain affected by plaques overlapped those areas affected in Alzheimer's disease, but other areas were involved. People after a head injury aremore likely to develop dementia, but it isn't clear why. Our findings suggest TBI leads to the development of the plaques which are a well-known feature of Alzheimer's disease."

People who suffer from TBI can have a slew of medical issues. While some TBI patients may experience cognitive impairments or difficulty with sensory information, others might have display mental health issues such as anxiety or depression. Yet, another long-term risk factor TBI patients is dementia. Scientists do not know the exact mechanism behind this relationship, but recent studies have made some progress into understanding it.


For the study, researchers recruited 9 people with an average age of 44 who had a single moderate to severe TBI. Their brain injuries had occurred between 11 months and 17 years previously. The research team took an in-depth look at their brains by taking PET and MRI scans. The PET scans detected amyloid plaques in the brain and the MRI scans searched out evidence of cellular damage resulting from the trauma.

The scan results were compared with 10 people with Alzheimer's disease and nine healthy participants (control group).

Both the people with brain injuries and the people with Alzheimer's disease had plaques in the posterior cingulate cortex, which is affected early in Alzheimer's. The researchers also found that plaques were increased in patients with more damage to the brain's white matter.

Interestingly, the TBI group, but not the Alzheimer's group, also showed plaques in the cerebellum.
Prof. Sharp said:

"It suggests that plaques are triggered by a different mechanism after a traumatic brain injury."
"The areas of the brain affected by plaques overlapped those areas affected in Alzheimer's disease, but other areas were involved.
“It suggests that plaques are triggered by a different mechanism after a traumatic brain injury. The damage to the brain's white matter at the time of the injury may act as a trigger for plaque production."

The current study is a relatively small-scale trial, however, Prof. Sharp believes that if a substantial link can be found between brain injury and the onset of Alzheimer's disease, it might help neurologists uncover treatment and prevention strategies to reduce the progression of Alzheimer's at an earlier stage.

Growth factor in brain may slow cognitive decline


A new study has found that older people with higher amounts of a key protein from the gene called brain-derived neurotrophic factor, or BDNF in their brains have slower decline in their memory and cognitive skills compared to people with lower amounts of protein from the gene.

People tend to experience decline in physical skills as they age. Although the physical decline is obvious, the brain also has a tendency to slow down.

Read more Blocking brain inflammation stops Alzheimer’s


Growth factor in brain may slow cognitive decline

However, it is not certain that cognitive decline will occur in all older adults. When it does occur, the speed of decline may vary from person to person. Significant impairment can be seen in some individuals, while others may show virtually no change at all.

The reasons behind these neurological differences are mystery to scientists. Since ageing is a multifaceted process and the brain is a complex organ, clues to the causal factors of mental decline with age are difficult to connect.

Dr.Aron S. Buchman and colleagues at the Rush University Medical Center in Chicago, IL, aimed to explore the involvement of BDNF in age-based cognitive decline.

BDNF is a growth factor that encourages the growth of new neurons and synapses, and supports existing neurons. It can be found extensively in both the brain and the peripheral nervous system. Many studies have shown that it is crucial in various important operations, including the maintenance of long-term memories.
Much of the nervous system in mammals is arranged before birth, but parts of the brain retain the ability to grow new neurons in a process called neurogenesis. BDNF is one of the major participants in this creation of new brain substance.

Read more Scientists identify vital early warning of Alzheimer’s that could lead to improved treatment

The role of BDNF in memory and the protection and development of neurons make it a key candidate for examinations into the cognitive decline seen in many ageing brains.

Rats born without the ability to create BDNF die soon after birth because of neural abnormalities. However, if BDNF is injected into the lateral ventricle of an adult rat, new neurons grow in the striatum, septum, thalamus and hypothalamus.

For the study, researchers recruited 535 people with an average age of 81. These participants were part of the Rush Memory and Aging Project and the Religious Orders Study. They were followed until death, for an average of six years. The participants took yearly tests of their thinking and memory skills, and after death, a neurologist reviewed their records and determined whether they had dementia, some memory and thinking problems called mild cognitive impairment or no thinking and memory problems. Autopsies were conducted on their brains after death, and levels of the gene that codes for BDNF in the brain were measured.

The rate of cognitive decline was about 50% slower for those in the highest 10% of protein from BDNF gene expression compared to the lowest 10%. The effect of plaques and tangles – 2 hallmarks of Alzheimer’s disease –reduced cognitive decline in people with high levels of BDNF. Cognitive decline was about 40% slower for people with the highest amount of protein from BDNF gene expression compared to those with the lowest amount.

On average, thinking and memory skills declined by about 0.10 units per year on the tests. Higher levels of protein from BDNF gene expression reduced the effect of plaques and tangles in the brain on cognitive decline by 0.02 units per year.

The researchers found that the plaques and tangles in the brain accounted for 27% of the variation in cognitive decline, demographics accounted for 3% and BDNF accounted for 2%.

Plaques and tangles can be found in the brains of people with Alzheimer’s. Scientists believe that the plaques and tangles negatively impact cognitive function. The study revealed that the effect of these markers on cognitive decline was reduced by 40% for individuals with the highest levels of BDNF.

Dr. Buchman said:
"This relationship was strongest among the people with the most signs of Alzheimer's disease pathology in their brains.

This suggests that a higher level of protein from BDNF gene expression may provide a buffer, or reserve for the brain and protect it against the effects of the plaques and tangles that form in the brain as a part of Alzheimer's disease."

Buchman noted that the study does not prove that BDNF is the cause of a slower rate of cognitive decline; further work is needed to determine if activities which increase brain BDNF gene expression levels protect or slow the rate of cognitive decline in old age.

The study was published in the online issue of Neurology, the medical journal of the American Academy of Neurology.