Friday 3 May 2024
Boosting Brain Power: Can Brain Training Really Enhance Cognitive Function?
Monday 11 December 2023
The Excessive TV-Watching will cause Dementia, Depression and Parkinson’s Disease
Monday 31 July 2023
Snoring Could Be Harming Your Brain
Monday 12 June 2023
The Role of Multivitamins in Memory Boost and Slowing Cognitive Aging
Sunday 23 April 2023
Had COVID? Part of the Virus May Stick Around in Your Brain
If you or someone you know is experiencing "brain
fog" after COVID-19, scientists now have a possible explanation — and it
might not bring much comfort.
Researchers in Germany found that part of the virus, the
spike protein, remains in the brain long after the virus clears out.
These investigators discovered the spike protein from the
virus in brain tissue of animals and people after death. The finding suggests
these virus fragments build up, stick around, and trigger inflammation that
causes long COVID symptoms.
About 15% of COVID patients continue to have long-term
effects of the infection despite their recovery, said senior study author Ali
Ertürk, PhD, director of the Institute for Tissue Engineering and Regenerative
Medicine at the Helmholtz Center Munich in Germany.
Reported neurological problems include brain fog, brain
tissue loss, a decline in thinking abilities, and problems with memory, he
said.
"These symptoms clearly suggest damages and long-term
changes caused by SARS-CoV-2 in the brain, the exact molecular mechanisms of
which are still poorly understood," Ertürk said.
The researchers also propose a way the spike protein can get
into the brain in their preprint report published online before peer review
April 5 on bioRxiv.
Delivered by circulating blood, the spike protein can stay
inside small openings in the bone marrow of the skull called niches. It can
also reside in the meninges, thin layers of cells that act as a buffer between
the skull and the brain. From there, one theory goes, the spike protein uses
channels to enter the brain itself.
The hope is researchers can develop treatments that block
one or more steps in this process and help people avoid long COVID brain
issues.
'Very Concerning'
"This is a very concerning report that literally
demonstrates the SARS-CoV-2 spike protein in the skull-meninges-brain axis in postmortem
individuals," said Eric Topol, MD, director of the Scripps Research
Translational Institute in La Jolla, CA, and editor-in-chief of Medscape,
WebMD's sister site for medical professionals.
Having the spike protein accumulate in structures right outside
the brain and causing ongoing inflammation makes sense to Topol. The clustering
of spike proteins would trigger an immune response from this niche reservoir of
immune cells that cause the inflammation associated with long COVID and the
symptoms such as brain fog, he said.
Problems with thinking and memory after COVID infection are
relatively common. One research team found 22% of people with long COVID
specifically reported this issue, on average, across 43 published studies. Even
people who had mild COVID illness can develop brain fog later, Ertürk and
colleagues note.
So why are researchers blaming the spike protein and not the
whole COVID virus? As part of the study, they found SARS-CoV-2 virus RNA in
some people after death and not in others, suggesting the virus does not need
to be there to trigger brain fog. They also injected the spike protein directly
into the brains of mice and showed it can cause cells to die.
Researchers also found no SARS-CoV-2 virus in the brain
parenchyma, the functional tissue in the brain containing nerve cells and
non-nerve (called glial) cells, but they did detect the spike protein there.
Surprising Findings
Investigators were surprised to find spike protein in the
skull niches of people who survived COVID and died later from another cause.
Ertürk, lead author and PhD student Zhouyi Rong, and their colleagues found
spike protein in 10 of 34 skulls from people who died from non-COVID causes in
2021 and 2022.
They also found COVID can change how proteins act in and
around the brain. Some of these proteins are linked to Parkinson's disease and
Alzheimer's disease, but have never before been linked to the virus
Another unexpected finding was how close the findings were
in mice and humans. There was a "remarkable similarity of distribution of
the viral spike protein and dysregulated proteins identified in the mouse and
human samples," Ertürk said.
Future Treatments?
Tests for protein changes in the skull or meninges would be
invasive but possible compared to sampling the parenchyma inside the brain.
Even less invasive would be testing blood samples for altered proteins that
could identify people most at risk of developing brain complications after
COVID illness.
It will take more brain science to get there.
"Designing treatment strategies for these neurological symptoms requires
an in-depth knowledge of molecules dysregulated by the virus in the brain
tissues," Ertürk said.
Wednesday 22 March 2023
Parkinson Disease
Parkinson disease (PD) is one of the most common neurologic disorders, affecting approximately 1% of individuals older than 60 years and causing progressive disability that can be slowed, but not halted, by treatment. The 2 major neuropathologic findings in Parkinson disease are loss of pigmented dopaminergic neurons of the substantia nigra pars compacta and the presence of Lewy bodies and Lewy neurites.
Signs and symptoms
Initial clinical symptoms of Parkinson disease include the following:
- Tremor
- Subtle decrease in dexterity
- Decreased arm swing on the first-involved side
- Soft voice
- Decreased facial expression
- Sleep disturbances
- Rapid eye movement (REM) behavior disorder (RBD; a loss of normal atonia during REM sleep)
- Decreased sense of smell
- Symptoms of autonomic dysfunction (eg, constipation, sweating abnormalities, sexual dysfunction, seborrheic dermatitis)
- A general feeling of weakness, malaise, or lassitude
- Depression or anhedonia
- Slowness in thinkin
Onset of motor signs include the following:
- Typically asymmetric
- The most common initial finding is a resting tremor in an upper extremity
- Over time, patients experience progressive bradykinesia, rigidity, and gait difficulty
- Axial posture becomes progressively flexed and strides become shorter
- Postural instability (balance impairment) is a late phenomenon
Nonmotor symptoms
Nonmotor symptoms are common in early Parkinson disease. Recognition of the combination of nonmotor and motor symptoms can promote early diagnosis and thus early intervention, which often results in a better quality of life.
Diagnosis
Parkinson disease is a clinical diagnosis. No laboratory biomarkers exist for the condition, and findings on routine magnetic resonance imaging and computed tomography scans are unremarkable.
Clinical diagnosis requires the presence of 2 of 3 cardinal signs:
- Resting tremor
- Rigidity
- Bradykinesia
Management
The goal of medical management of Parkinson disease is to provide control of signs and symptoms for as long as possible while minimizing adverse effects.
Symptomatic drug therapy
- Usually provides good control of motor signs of Parkinson disease for 4-6 years
- Levodopa/carbidopa: The gold standard of symptomatic treatment
- Monoamine oxidase (MAO)–B inhibitors: Can be considered for initial treatment of early disease
- Other dopamine agonists (eg, ropinirole, pramipexole): Monotherapy in early disease and adjunctive therapy in moderate to advanced disease
- Anticholinergic agents (eg, trihexyphenidyl, benztropine): Second-line drugs for tremor only
Treatment for nonmotor symptoms
- Sildenafil citrate (Viagra): For erectile dysfunction
- Polyethylene glycol: For constipation
- Modafinil: For excessive daytime somnolence
- Methylphenidate: For fatigue (potential for abuse and addiction)
Deep brain stimulation
- Surgical procedure of choice for Parkinson disease
- Does not involve destruction of brain tissue
- Reversible
- Can be adjusted as the disease progresses or adverse events occur
- Bilateral procedures can be performed without a significant increase in adverse events
Prognosis
Before the introduction of levodopa, Parkinson disease caused severe disability or death in 25% of patients within 5 years of onset, 65% within 10 years, and 89% within 15 years. The mortality rate from Parkinson disease was 3 times that of the general population matched for age, sex, and racial origin. With the introduction of levodopa, the mortality rate dropped approximately 50%, and longevity was extended by many years. This is thought to be due to the symptomatic effects of levodopa, as no clear evidence suggests that levodopa stems the progressive nature of the disease.
The American Academy of Neurology notes that the following clinical features may help predict the rate of progression of Parkinson disease :
Older age at onset and initial rigidity/hypokinesia can be used to predict (1) a more rapid rate of motor progression in those with newly diagnosed Parkinson disease and (2) earlier development of cognitive decline and dementia; however, initially presenting with tremor may predict a more benign disease course and longer therapeutic benefit from levodopa
A faster rate of motor progression may also be predicted if the patient is male, has associated comorbidities, and has postural instability/gait difficulty (PIGD)
Older age at onset, dementia, and decreased responsiveness to dopaminergic therapy may predict earlier nursing home placement and decreased survival
Patient Education
Patients with Parkinson disease should be encouraged to participate in decision making regarding their condition. In addition, individuals and their caregivers should be provided with information that is appropriate for their disease state and expected or ongoing challenges. Psychosocial support and concerns should be addressed and/or referred to a social worker or psychologist as needed.
Prevention of falls should be discussed. The UK National Institute for Health and Clinical Excellence has several guidance documents including those for patients and caregivers.
Other issues that commonly need to be addressed at appropriate times in the disease course include cognitive decline, personality changes, depression, dysphagia, sleepiness and fatigue, and impulse control disorders. Additional information is also often needed for financial planning, insurance issues, disability application, and placement (assisted living facility, nursing home).
Wednesday 4 December 2019
Scientists have finally decoded the bizarre behaviors of brain cells — and recreated them in tiny computer chips.
The tiny neurons could change the way we build medical devices because they replicate healthy biological activity but require only a billionth of the energy needed by microprocessors, according to a University of Bath press release.
Neurons behave similar to electrical circuits within the body, but their behavior is less predictable — especially when it comes to parsing the relationship between their input and output electrical impulses. But these new artificial brain cells successfully mimic the behavior of rat neurons from two specific regions of the brain, according to research published Tuesday in Nature Communications.
“Until now neurons have been like black boxes, but we have managed to open the black box and peer inside,” University of Bath physicist Alain Nogaret said in the release. “Our work is paradigm changing because it provides a robust method to reproduce the electrical properties of real neurons in minute detail.”
The ultimate goal is to use these neurons to build medical devices that can better cater to patients’ needs, like a smarter pacemaker that can respond to new stressors and demands on a person’s heart — essentially upgrading devices to be more in tune with the body.
Julian Paton, a physiologist at the universities of Auckland and Bristol, said in the release that recreating biological activity was exciting because it “opens up enormous opportunities for smarter medical devices that drive towards personalized medicine approaches to a range of diseases and disabilities.”
Wednesday 11 September 2019
We might soon be able to communicate telepathically
At least, that’s the gist of a new report about neural implant technology by the Royal Society, that was reviewed by The Independent. The document hypes some of the more exciting things brain-computer interfaces could make possible, but also warns that brains hooking to the computers ( watching too many SciFi movies!!) could also compromise individual privacy.
“Not only thoughts, but sensory experiences, could be communicated from brain to brain,” the report reads. “Someone on holiday could beam a ‘neural postcard’ of what they are seeing, hearing or tasting into the mind of a friend back home.” - Little bit of exaggeration.... Do you guys think that way?
To make sure that these neural implants of the future are used to benefit people and society, the Royal Society is calling for a government probe into the tech, The Independent reports. Otherwise, companies like Facebook and Tweeter that are already working on their own systems will be able to dictate how the tech is used on their own terms.
“They could bring huge economic benefits to the UK and transform sectors like the NHS, public health and social care,” report co-chair Christofer Toumazou from Imperial College of London told The Independent. “But if developments are dictated by a handful of companies then less commercial applications could be side-lined. That is why we are calling on the government to launch a national investigation”
READ MORE: Brain-Computer Interface Will Make People Telepathic, Scientists Say [The Independent]