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This talk introduces
Alzheimer's disease pathology,
using it as a basis for
further exploration of
the underlying
pathological features
of Alzheimer's disease,
including amyloid beta plaques,
tu neurofibrillary tangles,
neuro inflammation,
and vascular factors.
We will discuss how these
mechanisms interact
to drive cognitive decline
and neuronal loss.
The multifactorial nature of
the disease explains the
difficulty in developing
effective therapies and
highlights the importance of
a holistic combination approach
to treatment and
early detection.
Alzheimer's disease is
the most common cause
of dementia worldwide,
defined by progressive
cognitive decline
and memory impairment.
The disorder is marked
by brain atrophy,
widespread neuronal
and synaptic loss,
extracellular amyloid
beta plaques,
and intracellular
neurofibrillary tangles
from hyperphosphorylated
tau protein.
Neuro inflammation,
vascular factors,
and other mechanisms
play key roles,
making therapy difficult and
highlighting the need for
a multifactorial approach.
A defining feature of
Alzheimer's disease
is the formation of
neurofibrillary tangles,
aggregates of abnormally
phosphorylated
tau protein within neurons.
Normally tau stabilizes
axonal microtubules,
but in Alzheimer's,
it detaches, becomes
hypophosphorlated,
and forms paired
helical filaments.
These tangles disrupt
neuronal transport,
leading to dysfunction
and death.
Their spread follows a
predictable brain pattern,
