Neuroplasticity

Abstract

The real story of how our brains and nervous systems change throughout our lifetimes—with or without “brain training.” Fifty years ago, neuroscientists thought that a mature brain was fixed like a fly in amber, unable to change. Today, we know that our brains and nervous systems change throughout our lifetimes. This concept of neuroplasticity has captured the imagination of a public eager for self-improvement—and has inspired countless Internet entrepreneurs who peddle dubious “brain training” games and apps. In this book, Moheb Costandi offers a concise and engaging overview of neuroplasticity for the general reader, describing how our brains change continuously in response to our actions and experiences. Costandi discusses key experimental findings, and describes how our thinking about the brain has evolved over time. He explains how the brain changes during development, and the “synaptic pruning” that takes place before brain maturity. He shows that adult brains can grow new cells (citing, among many other studies, research showing that sexually mature male canaries learn a new song every year). He describes the kind of brain training that can bring about improvement in brain function. It's not gadgets and games that promise to “rewire your brain” but such sustained cognitive tasks as learning a musical instrument or a new language. (Costandi also notes that London cabbies increase their gray matter after rigorous training in their city's complicated streets.) He tells how brains compensate after stroke or injury; describes addiction and pain as maladaptive forms of neuroplasticity; and considers brain changes that accompany childhood, adolescence, parenthood, and aging. Each of our brains is custom-built. Neuroplasticity is at the heart of what makes us human.

Synapse Pruning: Mitochondrial ROS with Their Hands on the Shears

“…At birth, the developing brain makes ≈2 million synapses per minute . Precocious synaptogenesis establishes an immature connectome with considerable redundancy, such that, surplus synaptic inputs form in every major brain region from the cerebellum to the cerebral cortex .…”

“…As Blagosklonny enunciates most developmental programmes never truly cease, such that, aging is the proposed outcome of incessant “pseudo‐programing.” It is informative to view synapse pruning through such a theoretical prism. Using mitochondrial O 2 .− /H 2 O 2 to execute an essential developmental process is beneficial—as the advantages of pruning attest . However, a mitochondrial O 2 .− /H 2 O 2 defined pruning signal never truly ceases, it can only be temporarily suppressed (either by neuronal activity, high ATP demand or rebuffed by finite “silencing” programmes).…”

“…At birth, the developing brain makes %2 million synapses per minute. [6] Precocious synaptogenesis establishes an immature connectome with considerable redundancy, [7] such that, surplus synaptic inputs form in every major brain region from the cerebellum to the cerebral cortex. [8] Forming surplus synaptic inputs enables the developing brain to refine its burgeoning connectome by strengthening efficient while simultaneously weakening and removing inefficient synaptic inputs, respectively (termed synapse pruning-comprehensively reviewed in [7] ).…”

“…Using mitochondrial O 2 .À /H 2 O 2 to execute an essential developmental process is beneficial-as the advantages of pruning attest. [6,9] However, a mitochondrial O 2 .À /H 2 O 2 defined pruning signal never truly ceases, it can only be temporarily suppressed (either by neuronal activity, high ATP demand or rebuffed by finite "silencing" programmes [101] ). Mitochondria perpetually reside on the cusp of significant O 2 .À /H 2 O 2 production because of how they produce O 2 .À /H 2 O 2 (see section 4).…”

“…Applying the basic mechanisms of mitochondrial ROS production to an active and inactive synapse (see section [3][4][5] reveals that: mitochondrial ROS are endogenous synaptic activity sentinels because neuronal activity decreases whereas inactivity increases their production. Mechanistic links between mitochondrial ROS and intrinsic apoptosis, a known synapse pruning pathway, inform the novel hypothesis that: increased mitochondrial ROS production prunes inactive synapses by activating intrinsic apoptosis (see section [6][7][8]. Placing mitochondrial ROS with their hands on the shears, provides an overarching theoretical mechanism to explain seemingly disparate phenomena from how mitochondrial ROS: select weak synapses for pruning, bias pruning, cause aberrant pruning in pre-eclampsia and aging (see section [11][12][13].…”