Phylogenetic disorders of brain

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Topic:- Phylogenetic disorders of brain
By:- Tiwari Shivani
Group:- 191A
Guided by :- Zhukova Anna

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PHYLOGENETIC
DISORDERS OF BRAIN

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PHYLOGENESIS
BRAIN
EVOLUTION OF THE BRAIN
Alzheimer's disease
Parkinson's disease
Reference

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• the evolutionary development
and diversification of a species
or group of organisms, or of a
particular feature of an
organism.
• Phylogentics:- relating to the
evolutionary development and
diversification of a species or
group of organisms, or of a
particular feature of an
organism.

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• The brain is one of the largest and most complex organs in
the human body. It is made up of more than 100 billion
nerves that communicate in trillions of connections called
synapses. The brain is made up of many specialized areas
that work together: • The cortex is the outermost layer of
brain cells.
• The adult human brain weighs on average about 1.5 kg (3.3
lb). In men the average weight is about 1370 g and in women
about 1200 g. The volume is around 1260 cm3 in men and
1130 cm3 in women, although there is substantial individual
variation.

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• As a number, a “petabyte”
means 1024 terabytes or
a million gigabytes, so the
average adult human
brain has the ability to
store the equivalent of 2.5
million gigabytes digital
memory.
• Average weight
• 1400 grams

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• Alzheimer's disease is an
irreversible, progressive brain
disorder that slowly destroys
memory and thinking skills
and, eventually, the ability to
carry out the simplest tasks.
• The study finds evidence that
50,000 to 200,000 years ago,
natural selection drove
changes in six genes involved
in brain development.

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• Neurons in certain association areas of the human brain retain
juvenile characteristics into adulthood, such as the increased
expression of genes related to synaptic activity and plasticity,
incomplete myelination and elevated aerobic metabolism, which can
cause an increase in oxidative stress in these neurons. Oxidative
stress can cause myelin breakdown and epigenetic changes in the
promoter region of genes related to synaptic plasticity, reducing their
expression. These changes may in some cases induce
hyperphosphorylation of tau and β-amyloid deposits, which are
characteristic of AD. The adaptation of humans to the cognitive
niche probably required an increase in synaptic plasticity and activity
and neuronal metabolism in neurons in areas related to certain
cognitive functions such as autobiographical memory, social
interaction and planning.

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The cost of these changes may
have been the brain's increased
vulnerability to factors which can
trigger AD. This vulnerability may
have resulted from the
evolutionary legacies that have
occurred over the course of the
evolution of the human brain,
making AD a possible example of
antagonistic pleiotropy. The
evolutionary approach allows
apparently unrelated data from
different disciplines to be
combined in a manner that may
lead to an improved
understanding of complex
diseases such as Alzheimer's.

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• Parkinson's disease is a
progressive nervous
system disorder that
affects movement.
Symptoms start gradually,
sometimes starting with a
barely noticeable tremor
in just one hand. Tremors
are common, but the
disorder also commonly
causes stiffness or
slowing of movement.

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• There are two central premises to this evolutionary view of
Parkinson disease (PD). First, PD is a specific human disease.
Second, the prevalence of PD has increased over the course of
human history. Several lines of evidence may explain why PD
appears to be restricted to the human species. The major
manifestations of PD are the consequence of degeneration in the
dopamine-synthesizing neurons of the mesostriatal neuronal
pathway. It is of note the enormous expansion of the human
dopamine mesencephalic neurons onto the striatum compared with
other mammals. Hence, an evolutionary bottle neck was reached
with the expansion of the massive nigrostriatal axonal arborization.
This peculiar nigral overload may partly explain the selective fragility
of the human dopaminergic mesencephalic neurotransmission and
the unique presence of PD in humans.

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• On the other hand, several facts may explain the increasing
prevalence of PD over the centuries. The apparently low prevalence
of PD before the twentieth century may be related to the shorter life
expectancy and survival compared to present times. In addition,
changes in lifestyle over the course of human history might also
account for the increasing burden of PD. Our hunter-gatherers
ancestors invested large energy expenditure on a daily basis, a
prototypical physical way of life for which our genome remains
adapted. Technological advances have led to a dramatic reduction
of physical exercise. Since the brain release of neurotrophic factors
(including brain-derived neurotrophic factor) is partially exercise
related, the marked reduction in exercise may contribute to the
increasing prevalence of PD.

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