Extensive research has established the two most prominent pathological hallmarks in AD brains: senile plaques and neurofibrillary tangles (NFTs).
A potential problem underlying the failure to treat AD in humans is the assumption that senile plaques, the most obvious pathological hallmark of the disease, and especially one of the plaque components Aβ peptide represent the major driving force of the disease.
Although characterised by specific attributes and pathological hallmarks, most neurodegenerative diseases have features of mitochondrial dysfunction, which converge in metabolic alterations that ultimately lead to neuronal cell death and affect the brain physiology.
Recently, an Asn/Gln rich C-terminal segment of TDP-43 has been shown to produce aggregation in vitro and reproduce most of the protein's pathological hallmarks in cells, but little is known about this segment's structure.
Mutations within or multiplications of the gene encoding α-syn are known to cause genetic forms of PD and polymorphisms in the gene are recently established risk factors for idiopathic PD. α-syn is a major component of Lewy bodies, the intracellular proteinaceous inclusions which are pathological hallmarks of most forms of PD.
The accumulation of misfolded proteins in insoluble aggregates within the neuronal cytoplasm is one of the common pathological hallmarks of most adult-onset human neurodegenerative diseases.
While FUS and TDP-43 are normally located in the nucleus, FUS-positive and TDP-43-positive cytoplasmic inclusions are pathological hallmarks of most non-SOD1 sALS cases and a related neurological disorder, frontotemporal lobar degeneration (FTLD) (9, 14– 14).
The most elaborate insight with regard to the association with pathological hallmarks and disease progression has been obtained for AD.
Alzheimer's disease (AD) is one of the most devastating neuro-degenerative disorders characterized by the two pathological hallmarks of amyloid plaques and neurofibrillary tangles.
The major pathological hallmarks of multiple sclerosis (MS) comprise inflammation, demyelination with associated gliosis and axonal damage, which most likely correlates with persisting disability.
