Central Nervous System

The central nervous system (CNS) consists of the brain and spinal cord and
comprises neurons, neuronal processes, supporting cells of the CNS (glial cells), and
blood vessels. The CNS is invested with meninges and is suspended in cerebrospinal
fluid (CSF) which is produced by specialized choroid plexus structures. All parts of the
CNS are made up of grey matter (cell bodies and dendrites) and white matter (axons).
Neuroglia is masses of support cells where the neurons are embedded, and this forms
almost half of the total mass of the CNS. There are four principal types of neuroglia: (i)
Oligodendrocytes are equivalent to the Schwann cells of the peripheral nervous
system (PNS), and both are responsible for the formation of myelin sheaths in the CNS,
(ii) Astrocytes provide mechanical support and mediates the exchange of metabolites
between neurons and the vascular system. They form part of the blood-brain barrier.
Also, it plays an important role in the repair of CNS tissue after damage, (iv) Microglia
have defense and immunological functions, and (v) Ependymal cells line the ventricles
and spinal canal.

The most common progressive generalized deterioration of brain function is

dementia, particularly Alzheimer's dementia. There are two possibilities that can result
to Alzheimer's disease. The first one is Beta-Amyloid Plaque Formation. Beta-amyloid
is a protein fragment snipped from an amyloid precursor protein. APP can undergo
cleavage in three different locations: (1) At the N-terminal of the beta-amyloid domain
via beta-secretase, (2) Within the beta-amyloid domain via alpha-secretase, (3) At the
C-terminal of the beta-amyloid domain via gamma-secretase. However, the enzyme that
cuts APP into beta-amyloid (beta-secretase) could be more precise, this will result in
somehow larger strands that are insoluble. The resulting longer strands are very ‘sticky’
which will then clump into the deposits referred to as plaques (Bright Focus Foundation,
2020). The other one is the Neurofibrillary Tangles. These are accumulations of
abnormally phosphorylated tau protein within the perikayral cytoplasm of certain
neurons (Perl, n.d.). These are caused by the build-up of beta-amyloid plaques that
initiates pathways inside the neuron that leads to the activation of kinase, an enzyme
that transfers a phosphate group to the protein. Due to phosphorylation, Tau protein
undergoes modification such as changing in shape, then it will result in a halt in
supporting the microtubules, and clumps up with other tau proteins, or gets tangled.
When neurons are tangled, non-functioning microtubules can’t signal efficiently. This
would undergo apoptosis or programmed cell death.
References:

Amyloid Plaques and Neurofibrillary Tangles. (2020, March 13). Bright Focus

Foundation. https://www.brightfocus.org/alzheimers-disease/infographic/amyloid-

plaques-and-neurofibrillary-tangles

O'Dowd, G., Woodford, P., & Young, B. (2023). Wheater's Functional Histology (6th

ed.). ELSEVIER.

Perl, D. P. (n.d.). Neuropathology of Alzheimer’s Disease. PubMed Central

(PMC). Retrieved August 5, 2021, from

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2918894/