8

Bioinformatics of the Brain

diseases such as Alzheimer’s and Parkinson’s findings related to increased ox-

idative damage to macromolecules in CNS have been observed [31, 32]. Reac-

tive oxygen species cause an increase in cholinesterase and tyrosinase activities

in cortical neurons and nerve cells in the CNS to prevent cholinergic trans-

mission [33]. Consequently, it increases oxidative stress and neuronal death

leading to neurodegeneration. The primary distinction that sets these illnesses

apart from one another is the diversity of cells or tissues that are affected by

the conditions as they progress. For instance, in Parkinson’s disease (PD),

dopaminergic neurons in the substantia nigra are severely injured whereas

neurons in the brain and cortical region are unaffected. In Alzheimer’s dis-

ease (AD), on the other hand, widespread damage to neurons occurs in the

hippocampus and neocortex. Currently, neurodegenerative diseases have no

known cure, and strategies to delay the progression of the condition are often

employed in the clinics [30].

Neurodegeneration is a series of events in which neurons in the human

brain are directly affected resulting in the loss of neural function. A ma-

jor contributing factor to this consequence is the inability of neurons to re-

generate [34]. In such diseases, brain regions including the cerebral cortex,

cerebellum, and thalamus are severely affected in disease-specific patterns.

Neurodegenerative diseases arise from the contribution of diverse factors of

environmental (diet, age and exercise), metabolic stress, neuroinflammation,

neurovascular coupling and genetics (GWAS sex-linked inheritance) leading

to loss of neurons and synapses, and alteration of the key pathways [35, 36].

These alterations manifest as physical symptoms such as exhaustion, contrac-

tions, amnesia, and issues with movement [34].

1.6.1

Alzheimer’s Disease (AD)

Alzheimer’s disease (AD) is a progressive neurodegenerative disease marked

by diminished cognitive abilities, difficulties in self-care, and a variety of be-

havioral and neuropsychiatric abnormalities. It is caused by the loss of neurons

and synapses in the different regions of the CNS [37].

There are two types of diagnostic criteria for AD: The Diagnostic and

Statistical Manual (DSM) criterion and the one created by the National Insti-

tute of Neurological and Communication Diseases and the Stroke-Alzheimer

Disease and Associated Diseases Association (NINCDSADRDA) [38]. These

criteria can be used to evaluate and confirm the diagnosis of AD. Evaluations

include determining whether the patient has learning and memory disorders,

aphasia, apraxia, agnosia, impairment in executive functions (e.g., planning,

organizing, sequencing, abstraction), and whether there is any other CNS-

related pathology [39]. A variety of imaging modalities, including positron

emission tomography (PET), single photon emission tomography (SPECT),

magnetic resonance imaging (MRI imaging), and computed tomography (CT)

are utilized to rule out other potential causes and differentiate AD from other

brain disorders [40].