Category Archives: Neuro-Psych

Zombie Mice Brain Cells: Clearance Stops Cognitive Decline

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Bodies, both mice and human, have a natural anti-cancer defense. Cells which have accumulated so many mutations that might lead to uncontrolled growth (i.e., cancer) move into senescent mode; they cease dividing and are eventually eliminated by the immune system.

Recently published research on mice has demonstrated the rather striking finding occurring when clearing or flushing all senescent cells from the brains of mice genetically bred to exhibit signs of dementia: “When senescent cells were removed, we found that the diseased animals retained the ability to form memories, eliminated signs of inflammation, did not develop [protein] tangles, and had maintained normal brain mass.”

Below are links to three media articles on the work, together with a link to the research article abstract.

Removing faulty brain cells staves off dementia in mice
Over-the-hill cells may cause trouble in the aging brain
Zombie cells found in brains of mice prior to cognitive loss
Research abstract:
Clearance of senescent glial cells prevents tau-dependent pathology and cognitive decline

All links have been added to
Alzheimer’s > Neurology & Neuroplasticity

Is It Possible Alzheimer’s Is An Infectious Disease?

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Although a “germ theory” approach to Alzheimer’s has occasionally be advocated for years, it has never developed the traction of a “major” approach to the disease. Recently, evidence has begun accumulating that certain viruses, particularly the HHV-6 and HHV-7 human herpes viruses may be involved in the development of Alzheimer’s, albeit in a complex way (see Herpes & Alzheimer’s and Herpes & Alzheimer’s — More). A new article discussing this together with a new initiatives to explore the “germ theory” approach to Alzheimer’s has just been published:

Two striking statistics cited in that article are the following:

All links have been added to Alzheimer’s > Neurology & Neuroplasticity

Herpes & Alzheimer’s — More

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Earlier this month, we described a study demonstrating a link between the presence of certain herpes viruses in the brain, and the presence of Alzheimer’s signs. Interestingly, three more studies of this connection have appeared. All three confirm this connection, but the third in addition suggests that aggressive treatment with herpes anti-viral medication can significantly reduce the chance of encountering dementia. However, the study did not attempt to deal with people who had already encountered dementia.

Here are two media articles:
Herpes linked to Alzheimer’s: Antivirals may help
Alzheimer’s risk 10 times lower with herpes medication

Here is an interesting scientific commentary by two researchers active in the area (referenced in both media articles linked above):
Herpes Viruses and Senile Dementia: First Population Evidence for a Causal Link

Here are links to the first two research studies
Increased risk of dementia following herpes zoster ophthalmicus
Epidemiology and long-term disease burden of herpes zoster and postherpetic neuralgia in Taiwan: a population-based, propensity score-matched cohort study

Here is the abstract of the third research article which provides information that “The usage of anti-herpetic medications in the treatment of HSV infections was associated with a decreased risk of dementia”:
Anti-herpetic Medications and Reduced Risk of Dementia in Patients with Herpes Simplex Virus Infections-a Nationwide, Population-Based Cohort Study in Taiwan.

All links have been added to Alzheimer’s > Risk Factors and Alzheimer’s > Neurology & Neuroplasticity

Herpes & Alzheimer’s

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For many years, theories have been proposed concerning the possible involvement of viruses with Alzheimer’s disease, but they have been seen as controversial. New research, based on examination of brain tissue from 1,000 deceased Alzheimer’s sufferers, has strengthened the case for some sort of link. The examination of those brains showed a much higher incidence of two strains of herpes virus than in the brains of deceased healthy controls. These two strains of herpes are extremely common, and typically begin life-long residence in the body and brain during childhood.

However, all scientists involved stress that it is unknown at present whether the presence of these viruses acts as triggers for Alzheimer’s, or whether the presence is a side-effect of Alzheimer’s.

Media articles on the work:
Researchers Find Herpes Viruses In Brains Marked By Alzheimer’s Disease
A Common Virus May Play Role in Alzheimer’s Disease, Study Finds
Childhood viruses linked to Alzheimer’s
Alzheimer’s link to herpes virus in brain, say scientists
The research article:
Multiscale Analysis of Independent Alzheimer’s Cohorts Finds Disruption of Molecular, Genetic, and Clinical Networks by Human Herpesvirus

All links have been added to Alzheimer’s > Neurology & Neuroplasticity

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