Category Archives: Neuro-Psych

New Biological Definition Of Alzheimer’s Advances

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Historically, Alzheimer’s Dementia (AD) has been defined by visible symptoms, simply because that was all that was available. Around the mid 1990’s, various researchers began pushing for the development of a biologically-based specification of the disease, separate from the manifested symptoms. Among other things, this allows reasoning about the onset of AD before manifestation of symptoms, much like cancer or heart disease. It is believed that the AD process may begin decades before any outward sign of memory loss or other decline.

In 2007, leading AD clinicians formed an international working group (IWG) and proposed using amyloid PET scans, MRI, CSF (cerebrospinal fluid) levels of Aβ and tau, genetic testing, brain structural changes, and subtle cognitive changes to diagnose AD at an earlier stage than before. The NIA/AA (National Institute of Aging, and the Alzheimer’s Association) set up a separate leadership group, and in 2011 it proposed a related set of diagnostic guidelines for AD research that utilized separate criteria for three stages of disease: preclinical AD, mild cognitive impairment, and dementia. The current NIA/AA research framework draws on these two efforts and their personnel.

The workers stress, both in the framework publication and in an associated editorial, that this work is directed at research, and will only slowly begin appearing in the clinical context. But it is expected that the new framework will markedly improve research communication and advances.

Links to media articles on the new framework:
New biological research framework for Alzheimer’s seeks to spur discovery
Alzheimer’s disease redefined: New research framework defines Alzheimer’s by brain changes, not symptoms
New Definition of Alzheimer’s Hinges on Biology, Not Symptoms

Links to two different publications of the framework:
NIA-AA Research Framework: Toward a biological definition of Alzheimer’s disease
NIA-AA Research Framework: Toward a biological definition of Alzheimer’s disease

All the links have been added to Neuro-Psych and to Alzheimers > Neurology & Neuroplasticity

Conflict! New Neurons or Not?

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Do human brains keep generating new neurons in the hippocampus throughout life, or not?

Two studies, just published within a month of each other, come down on opposite sides of that question.

The first link below is a well-written media article discussing the two research papers and the possible grounds for the conflict:
Do Older Brains Make New Neurons or Not?

Next are a link to a media article on the “no-new-neurons” work, together with the research abstract:
Your brain stopped making new cells at age 13, study claims
Human hippocampal neurogenesis drops sharply in children to undetectable levels in adults

And here is a link to a media article on the “new-neurons-all-through-life” work, together with a link to the full research article:
Surprise! Scientists find signs of new brain cells in adults as old as 79
Human Hippocampal Neurogenesis Persists throughout Aging

Finally, to give rats their due, here are links to a media article and to the research article, on work showing that strong physical exercise causes rat brains to increase the rate at which new hippocampal neurons are created:
Physical exercise increases adult hippocampal neurogenesis in male rats provided it is aerobic and sustained.
Sustained aerobic exercise increases adult neurogenesis in brain

All the links have been added to Neuro-Psych.

Maybe Flashing Lights For Alzheimer’s Therapy?

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Mice again, but not drugs. Instead, it’s the promising use of strobe-type flashing lights to modify brain waves (neuromodulation) to induce changes beneficial to Alzheimer’s sufferers.

It has been previously noted that both human Alzheimer’s sufferers and the mice models of Alzheimer’s exhibit disrupted gamma waves, which are the highest frequency waves and are associated with higher cognitive events. The study placed mice, genetically engineered to mimic Alzheimer’s symptoms, in a box with strobe lights flashing at 40 cycles per second for an hour a day. This stimulated the visual cortex of the mice to generate more gamma waves, which set in motion an apparent sequence of biological events: A change in gene expression causes microglia (immune cells in the brain) to change shape, going into scavenger mode, where they better perform their usual housekeeping role, clearing away cellular debris, including amyloid-β.

Note how complex the brain and how difficult the science: In Brain Inflammation & Alzheimer’s, we discussed work showing that Alzheimer’s-type inflammatory response on the part of microglia can lead to increase in the deposit of amyloid-β, whereas the present work shows the microglia being stimulated to improve the removal of amyloid-β.

Here is a link to a recent Nature magazine news feature article on the MIT work and related work on the role of brain waves. The article is an excellent explication of the work and how it affects how the brain works:
How flashing lights and pink noise might banish Alzheimer’s, improve memory and more

Below are links to a number of media articles on the work. The first group deals with the MIT group’s earlier report from 2016:
Flashing light therapy’ for Alzheimer’s
Beating Alzheimer’s With Brain Waves
Unique visual stimulation may be new treatment for Alzheimer’s
LED Lights May Be a Promising New Alzheimer’s Treatment, MIT Study Says
Toward Treating Alzheimer’s Disease with Brain Waves
Here is the earlier research article:
Gamma frequency entrainment attenuates amyloid load and modifies microglia

Here are links to media articles on the more recent research:
Alzheimer’s Memory Loss May Be Reversible, MIT Study Says
How does the Sp3-HDAC2 Complex Reduce Synaptic Function in Alzheimer’s?

And here is the more recent research report:
The Transcription Factor Sp3 Cooperates with HDAC2 to Regulate Synaptic Function and Plasticity in Neurons

Light therapy (sitting bathed in light every morning) has been successfully used for treating the form of depression known as Seasonal Affective Disorder (SAD) (see e.g., Take Light, Not Drugs). If this strobe-approach to Alzheimer’s is successful with humans, Alzheimer’s treatment could utilize a similar therapeutic approach, or even possibly the two therapies could be combined when appropriate.

All of the links have been added to Alzheimer’s > Treatment

Drug For Huntington’s, Maybe Later Alzheimer’s?

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Huntington’s disease is a neuro-degenerative disorder in which nerve cells in the brain are damaged. It is inherited, caused by defects in a single gene. Huntington’s effects include changes in behavior and emotions, involuntary jerky movements, and cognitive difficulties. To date there have been no effective drugs or other treatments. Consequently, there has been considerable excitement over the announcement of positive results of a Phase 1 trial of a drug for Huntington’s.

The drug is a synthetic single strand of DNA which has been customized to latch onto the Huntington messenger molecule, thereby blocking it’s action. There is excitement that similar custom DNA molecules could be created for Alzheimer’s and Parkinson’s. Needless to say, there is much hard work ahead.

Here are four media articles about the announcement (Publication will occur at a later date.):

Excitement as trial shows Huntington’s drug could slow progress of disease
Drug trial shows promising results to fight Huntington’s disease
Drug lowers deadly Huntington’s disease protein
First trials of Huntington’s drug show it could slow disease

All four links have been added to Neuro-Psych

Category: Neuro-Psych

Brain Inflammation & Alzheimer’s

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A current article, published on this year’s solstice (21 Dec), has excited Alzheimer’s researchers about the possibility of a refinement of the line of attack on the disease. The deposit of amyloid plaques is widely regarded as the core cause of the death of masses of brain neurons, the direct cause of Alzheimer’s symptoms. Most drug development efforts have targeted removal of the plaques, and almost all have failed (see The hard truth about Alzheimer’s drugs, link filed in Treatment > Drugs). The only one with any promise is Aducanumab, which only seems to have value if taken in very early stages of Alzheimer’s, and will be hugely expensive (see the article at end).

Besides the development of amyloid plaques, tangles of tau proteins inside the neurons, together with signs of activated/irritated immune cells called microglia are also found extensively in the brains of Alzheimer’s patients. The activated/irritated microglia can be caused by such things as a mild injury or a virus, and are also provoked by the deposit of amyloid. The newly published paper suggests that there may be an interaction or even feedback loop between deposit of amyloid and the irritated microglia. A key part of the process is the formation inside the microglia of a protein complex called an inflammasome. This complex both signals to other microglia to provoke further inflammation, but also releases specks of a protein called ASC. These specks appear to act as seeds for further deposit of amyloid, and the resulting amyloid plaques have ASC specks at their core. The first media article below compares this to the “grit inside a pearl”.

The research was mostly carried out on mice, though examining the brains of deceased Alzheimer’s patients showed substantial amounts of amyloid plaque containing ASC specs at core. In parts of the mice experiments, it was shown that presence or absence of ASC affected the generation of amyloid, and in other parts of the experiments, it was shown that when antibodies to ASC were injected, it interfered with the seeding effect for amyloid by ASC.

Thus, attacking inflammation and the action of ASC now seems like a promising way forward.

Here are two media articles about the study:

Brain inflammation sows the seeds of Alzheimer’s
Do Microglia Spread Aβ Plaques?

Here is the original study article:
Microglia-derived ASC specks cross-seed amyloid-β in Alzheimer’s disease

All three of these links have been added to Alzheimers > Neurology & Neuroplasticity

And here is an article about the drug Aducanumab (link added to Treatment > Drugs):
Robert Chen, MD-PhD candidate in Alzheimer’s research: What were the key findings from the Aducanumab phase 1 clinical trials? [Reprinted as: Aducanumab Is Showing Promise As An Alzheimer’s Treatment, But It’s Still Early]

Your Brain Sleeping: Locally Only?

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Most previous brain research about sleep has been oriented towards all-in, or all-out: fully asleep or completely awake. However, new research from MIT suggests that parts of the brain may be asleep while other parts are still awake. A link to the article has been posted on Strong Brain in Neuro-Psych:
How the brain controls sleep: Brain structure generates pockets of sleep within the brain Maybe this is what happens when we drift off at night and struggle to stay asleep in the morning?

Category: Neuro-Psych

New Neuroscience Links

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Here are the newest links in Neuroscience:

Important Link between the Brain and Immune System Found     New anatomical structures have been identified which form a network of lymphatic vessels in the meninges — the membranes that surround the brain and spinal cord — that shuttle fluid and immune cells from the cerebrospinal fluid to a group of lymph nodes in the neck

The Benefits of Nature Experience: Improved Affect and Cognition     
This study extends previous research by demonstrating additional benefits of nature experience on affect and cognition through assessments of anxiety, rumination, and a complex measure of working memory (operation span task).

Nature experience reduces rumination and subgenual prefrontal cortex activation     
This study reveals a pathway by which nature experience may improve mental well-being and suggests that accessible natural areas within urban contexts may be a critical resource for mental health in our rapidly urbanizing world.

The Brain: Our Strange, Important, Subconscious Light Detectors     
Sightless cells hidden within the eye may set our circadian rhythms, trigger migraines, and explain the seasonal ebb and flow of our moods.

‘I’m bad with names’ is a real thing     
Names are arbitrary and that meaninglessness makes it harder to hold the memory of it.

Blood turned into nerve cells by Canadian researchers     
Stem cells extracted from blood are converted into neural stem cells using patented technique

The Man Who Saw Time Stand Still     
One day, a man saw time itself stop, and as David Robson discovers, unpicking what happened is revealing that we can all experience temporal trickery too.

How to Use Light to Control the Brain     
Using “optogenetics,” researchers are able to trigger a memory