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The major pathological hallmarks of multiple sclerosis (MS) comprise inflammation, demyelination with associated gliosis and axonal damage, which most likely correlates with persisting disability.
The two major pathological hallmarks of AD are the progressive loss of cholinergic neural transmission, formation of a beta-amyloid plaques (Aβ-plaques) that forms senile plaques (SPs) and neurofibrillary tangles (NFTs) of hyperphosphorylated tau protein [4, 5].
The mechanism by which ApoE isoform affects risk of AD is uncertain, with roles proposed in all three of the major pathological hallmarks: Cell death [11], neurofibrillary tangles [12], [13] and senile plaques [3], [14].
The accumulation of Aβs (amyloid β-proteins) is one of the major pathological hallmarks in AD.
Synaptic loss is one of the major pathological hallmarks of AD.
The two major pathological hallmarks of AD are extracellular plaques and intracellular tangles.
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Abundant extraneuronal deposit of amyloid-beta (A β) is the major pathological hallmark and plays an early important pathologic role in the development of AD.
The major pathological hallmark of AD plays an early and important pathologic role in the development of AD.
The death of dopaminergic neurons is a major pathological hallmark of Parkinson's disease (PD).
The aggregates of α-synuclein (αS) are a major pathological hallmark of Parkinson's disease (PD) making their structure-function relationship important for rational drug design.
A major pathological hallmark of AD is the deposition of insoluble extracellular β-amyloid (Aβ) plaques.
Related(19)
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