Table 1.

Most common acute and chronic NDs, their clinical manifestations, and causes.

Disease	Clinical manifestations	Cause
Alzheimer's disease (AD)	Memory loss and cognitive decline.	Neuronal death that involves a vast area of the CNS, promoted by the deposition of amyloid‐β (Aβ) peptides into plaques [3].
Parkinson's disease (PD)	Motor and non-motor disorders, like tremors and delayed movement. Specifically, dyskinesia with resting tremors, muscle rigidity, and cognitive dysfunction [4].	Loss of dopaminergic neurons in the substantia nigra, nigrostriatal pathway degeneration [5,6]. α-synuclein positive inclusions in cell bodies and neurites (Lewy bodies) of nigral and olfactory bulb neurons [[7], [8], [9]]. Further, neuroinflammation and oxidative stress are involved [10,11].
Amyotrophic lateral sclerosis (ALS)	Muscles of the limbs, throat, tongue, and respiratory system gradually deteriorate and lose strength.	Degeneration of the upper motor neurons of the corticospinal tract and the lower motor neurons that control the skeletal muscles [12]. Mechanisms are still unclear, despite many studies demonstrating the involvement of several altered signaling pathways, such as mitochondrial dysfunction, glutamate excitotoxicity, oxidative stress, and neuroinflammation [13].
Multiple sclerosis (MS)	Severe physical disabilities.	Demyelinating disease caused by CNS inflammation and immune dysfunction [14].
Huntington's disease (HD)	Motor (involuntary movement disorder and impairment of voluntary movements), cognitive (problems of attention, cognitive slowing) and neuropsychiatric (depression, irritability, and apathy) disorders.	Autosomal dominant disorder caused by the elongation of CAG repeats on the short arm of chromosome 4p16.3 in the HTT gene. As per the proposed mechanisms, the degeneration of neurons in the putamen, caudate, and cerebral cortex, and the loss of substance-P-containing medium spiny neurons can be attributed to various factors. These include the accumulation of mutant protein aggregates, which impair the ubiquitin-proteosome pathway, transcriptional dysregulation, excitotoxicity caused by the increased release of glutamate and glutamate agonist, mitochondrial dysfunction, and altered energy metabolism, as well as changes in axonal transport and synaptic dysfunction [15,16].
Acute ischemic stroke (AIS)	Aphasia, agraphia, acalculia, apraxia, visual field deficit, hemiparesis, and hemisensory loss [17].	Neurodegeneration, cell death, changes in brain volume and cognitive performance consequent to the disruption of blood and oxygen flow [18].
Spinal cord injury (SCI)	Flaccid paresis, exclusively diaphragmatic respiration, low blood pressure, bradycardia, and loss of control of the urinary outlet [19].	Commonly results from a sudden, traumatic impact on the spine that fractures or dislocates vertebrae; following this primary injury, a secondary one starts and causes progressive damage to spinal cord tissue, impeding neurological recovery due to complex and interconnected cellular, molecular and biochemical phenomena [20].