What Is a Neuroplastician?

[CRG]

Psychology Today

What Is a Neuroplastician?


Key points

Neuroplasticity enhances learning and memory via new neural connections.
Brain recovery is possible in later stages of life, aiding injuries or diseases.
Neuroplasticians rewire brains, enabling better learning and habits.

Ever wanted to change habits? Emotional, psychological, or social, like overcoming anxiety or learning new skills? If so, you might benefit from the expertise of a neuroplastician.
What Exactly Is a Neuroplastician?

And how can they help you achieve lasting change? Let's discover how a neuroplastician can support you in building new healthy habits that sustain well-being.
But First: What Is Neuroplasticity?

Neuroplasticity is a concept that has transformed our understanding of the human brain. This is the capacity of the brain to change and adapt, even in adulthood, through the formation of new neural connections. Let’s start with two kinds of neuroplasticity:

A. Structural plasticity refers to the physical changes in the brain's structure, such as the growth of new neurons or the formation of new connections between existing neurons, which contribute to learning and memory.

B. Synaptic plasticity, on the other hand, involves the strengthening or weakening of existing connections between neurons, affecting the efficiency of neural communication.

Behavioral tools that drive neuroplasticity are all about B and include activities like learning new skills, practicing mindfulness, engaging in physical exercise, and adopting positive habits, all of which can promote the rewiring and adaptation of the brain for improved cognitive function and emotional well-being.

More of this nonsense at: https://www.psychologytoday.com/gb/blog/brain-reboot/202310/what-is-a-neuroplastician

Neuroplasticity without the babble: Adult Neuroplasticity: More Than 40 Years of Research

 

[Hutan]

More of this nonsense at:

I found that paper your recommend @CRG on Adult Neuroplasticity an interesting read. Clearly a lot of things remain to be worked out.

Here's some bits I found interesting before I ran out of steam:

Studies on the prefrontal cortex showed that neurons in this brain region are particularly plastic in that they change their dendritic morphology with the diurnal rhythm [10].

That means that any study of dendritic morphology in ME/CFS or depression or any chronic illness where people aren't necessarily following a normal diurnal rhythm needs to consider diurnal fluctuation.

In the late 1990s, there were reports that even the stress that an individual experiences can kill neurons in the brain. This message was based on studies in wild vervet monkeys that had been housed in a primate center in Kenya where they died suddenly. The animals had experienced severe stress because of social isolation from their group [16]. The finding that their brains revealed dead pyramidal neurons in the hippocampus attracted great public attention as the message was reduced to “stress kills neurons.” However, it later turned out that in this study on wild life animals the post mortem treatment of the brain tissue had been not optimal. The time between death of the animals and fixation of the brains for the neuropathological analysis was obviously too long so that morphology of the neurons was affected to an extent that had nothing to do with the previous stress exposure of the living animals. Since stress raises plasma glucocorticoids (GC), monkeys were chronically treated with GC in a subsequent study, and also the brains of these animals revealed changes in neuron morphology that were interpreted as dead or dying neurons [17].

However, these findings could not be confirmed by others. Instead, it was recognized that the morphological analysis of pyramidal neurons is technically delicate. It became apparent that, after a subject’s death, neurons may dramatically change their morphology and turn into “dark neurons” when the brain tissue has not been fixed adequately for the histological analysis [18]. When the chronic stress experiments were repeated under conditions that acknowledged those technical issues, it turned out that stress does not kill neurons, which is definitely a good message for stressed individuals [19]. Further studies showed that apoptosis (programmed cell death) in the hippocampal formation is a relatively rare event and that chronic stress may even reduce cell death in certain hippocampal subfields while increasing apoptosis in others [20]. Since chronic social stress in animals is regarded as preclinical model for depression the finding of a lack of neuron death in stressed animals also shed new light on a hypothesis saying that, in humans, major depression kills neurons in the brain. Indeed, it was later found that hippocampal neuron numbers in depressed subjects do not significantly differ from the numbers in healthy individuals [21].

Also the hypothesis that chronic GC [glucocorticoid] exposure leads to neuron death had to be revised. A summary of a range of studies on these issues concluded that it is unlikely that endogenous GC can cause structural damage to the hippocampal formation [22]. Nevertheless it is an established fact that “adverse influences” such as stress, depression, and chronic GC treatments may cause shrinkage of the hippocampal formation [23]. However, the underlying processes are obviously not neuron loss but other changes in the tissue such as reductions in neuronal dendrites and further presumptive alterations in the neuropil that have not been identified in detail yet ([6, 24]; for review see [25]).

Despite the 'established fact', the paper then casts some doubt on brain morphology findings related to depression - it seems rather unclear.

The most appealing phenomenon of neuroplasticity appears to be adult neurogenesis, that is the generation of new neurons in adult brains.
..
In the olfactory epithelium of the mammalian nose, sensory neurons are continuously generated throughout the lifespan, as first shown in adult squirrel monkeys [38]. This electron microscopic study clearly showed large numbers of newborn sensory neurons that are produced every day in the olfactory epithelium of the adult animals. Later it was found that also neurons in the olfactory bulb (OB) of adult mammals can be replaced.
..
However, OB neurogenesis is easier to detect than hippocampal neurogenesis and it took several years until there was reliable evidence that hippocampal neurogenesis does exist in adult mammals.

To detect neurogenesis in brains of adult humans the group of J. Frisén took advantage of the increased concentration of 14C in the atmosphere after nuclear bomb tests [54]. After a nuclear explosion, this radioisotope is increasingly incorporated into dividing cells of living organisms, including humans. Through the determination of 14C, the authors found that about 700 new neurons are generated daily in the hippocampal formation of adult humans. Interestingly, the 14C analysis of human brains revealed adult neurogenesis in the striatum, adjacent to a site at the lateral ventricle where neuronal precursor cells are generated, and there are indications that the neuroblasts in the human striatum differentiate to interneurons [55]. Surprisingly, no newborn neurons could be detected with the 14C technique in the adult human OB. These most recent findings clearly show that species and brain-region specific processes of neurogenesis await further elucidation.

The paper notes that some initial findings turned out to be wrong, due to technical difficulties, and that there is still a lot to be understood.