This article was written by
Ali Le Vere at Greenmedinfo.com. It’s republished here with their permission. For more information from Greenmedinfo, you can sign up for the newsletter
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Contrary to conventional
wisdom, brain regeneration is possible. One promising therapy that
promotes neurogenesis and is effective in pre-clinical studies of
Alzheimer’s and Parkinson’s is near infrared light therapy, and it may
improve other mental illnesses and neurodegenerative disorders including
dementia, stroke, ALS, and traumatic brain injury as well.
Alzheimer’s disease and Parkinson’s
disease are the most common neurodegenerative disorders. The former is a
type of dementia that occurs secondary to the accumulation of abnormal
protein deposits in the brain, including β-amyloid plaques and
intraneuronal neurofibrillary tangles made of tau protein (1). Upon
neuroimaging studies, gross cerebral cortical atrophy is found, meaning
that the part of the brain responsible for executive functions such as
learning, memory, language, decision-making, and problem-solving
progressively degenerates (1). In addition, gliosis, or brain
inflammation, is a hallmark characteristic of
Alzheimer’s (1).
One hypothesis that is championed
proposes that Alzheimer’s occurs due to self-propagating, prion-like
protein assemblies, which interfere with the function of nerve cells
(2). An alternate theory is that these so-called proteinopathies occur
secondary to a microvascular hemorrhage or brain bleed (3). The brain
bleed is believed to be the result of age-induced degradation of
cerebral capillaries, which creates neuron-killing protein plaques and
tangles (3).
Dysfunction of mitochondria, the
energy-generating powerhouses of the cell, is also implicated in
Alzheimer’s, as reduced efficacy of these organelles creates oxidative
stress-inducing reactive oxygen species, or free radicals, which lead to
neuronal cell death (4). Whatever the cause, extensive death of brain
cells occurs, which explains the cognitive deficits that occur with
Alzheimer’s disease, in addition to symptoms such as impaired judgment,
confusion, agitation, linguistic abnormalities, social withdrawal, and
even hallucinations (1).
Parkinson’s disease,
on the other hand, is characterized by progressive death of
dopamine-producing neurons in a region of the brainstem called the
substantial nigra, but it can extend to other brain areas such as the
locus coeruleus, olfactory bulb, dorsal motor nucleus of the vagal
nerve, and even the cortex in late stages (5). As a result, the primary
manifestation is that dopamine deficiency appears in the basal ganglia, a
set of nuclei embedded deep in the brain hemispheres that is
responsible for motor control (6). This leads to the cardinal
manifestation of Parkinson’s, namely, a movement disorder that includes
bradykinesia or slow movement, loss of voluntary movement, muscular
rigidity, and resting tremor (7).
Not unlike what happens in Alzheimer’s,
accumulation of abnormal intracellular protein aggregates known as Lewy
bodies, composed of a protein called α-synuclein, is thought to be
central to the pathogenesis of Parkinson’s disease (8). Like
Alzheimer’s, mitochondrial dysfunction induced by genetic mutations,
toxic agents, or damage to blood vessels is also considered to
contribute to
neuron cell death in
Parkinson’s (9). Toxin exposure is especially implicated, as animal
studies hint that development of Parkinson’s disease may occur as a
byproduct of exposure to neurotoxins such as rotenone or paraquat (10).
Impaired blood brain barrier function and damage to the endothelial
cells of the vascular system, which line the interior surface of blood
vessels, are also thought to play a role in Parkinson’s (10).
Overturning Old Notions of Neuroscience
The central dogma of neuroscience
conceived of the central nervous system tissue as “perennial” after the
doctrines of Giulio Bizzozero, the most prominent Italian histologist,
who decreed that the lifelong cells of the nervous system were devoid of
replicative potential (11). In other words, the perennial nature
ascribed to the nerve cells of the brain and spinal cord meant that
nerve cells were believed to be incapable of undergoing proliferation,
or cell division, in the postnatal brain (11). While the early stage of
in utero prenatal development known as embryogenesis permits massive
neurogenesis,
or the ability to create new nerve cells, the scientific consensus up
until the end of the twentieth century held that neurogenesis was
arrested after birth in mammals.
Santiago Ramon y Cajal, who led the
charge in the neuroscience discipline in the later half of the
nineteenth century onward and won a Nobel Prize for Medicine and
Physiology, in fact stated that: “Once development was ended, the fonts
of growth and regeneration of the axons and dendrites dried up
irrevocably. In adult centers, the nerve paths are something fixed and
immutable: everything may die, nothing may be regenerated” (11).
Acknowledgment of the mere possibility of adult neurogenesis was
hampered by the fact that scientists lacked the visualization techniques
to detect neural stem cells, the precursors to new neurons and means by
which neurogenesis occurs, and also did not have access to the
molecular markers and microscopy required to observe cells in different
cycle phases.
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