The research team found that the amount of tau protein
in the blood correlates to the amount accumulated in the brain.
Even so, accumulational soluble A[sz] oligomer can damage synaptic junction and generate neurovirulence. In pathology situation, the unbalance between the production and clearance rate of A[sz] can lead to its sedimentation, causing for AD to happen using tau protein
poisonousness, destroying intracellular calcium homeostasis and cholinergic nerve system, inducing neurofibrillary tangles (NFTs), etc., Hence reducing A[sz] deposition can improve AD of a large extent and make it possible the targeted therapy of AD in allusion to A[sz], such as A[sz] antibody and beta-secretase cleaving enzyme (BACE) inhibitor.
The results showed that a compound that boosts the function of the endosomal network significantly cuts the production of both amyloid beta and a precursor of the Tau protein
A[beta]P-42, tau protein
, [alpha]-synuclein, asialoganglioside [GM.sub.1], GFAP, rab-5, ATP-synthase, MBP, and their antibodies have been linked with neurodegeneration and diseases such as AD, Parkinson's disease (PD), and multiple sclerosis (MS) [2, 7-14].
PPIs and Tau Protein
. Currently, AD diagnosis is based on neuropsychological tests (cognitive criteria), neuroimaging (i.e., MRI and amyloid deposits by PET), and tau/amyloid in CSF (biomarker criteria) that rule out other causes of dementia [42-44].
The scientists investigated the role of ApoE in mice whose brains contained potentially toxic human tau protein
Since that time, almost all of the disease-modifying new drugs under development are targeting A[beta] or Tau protein
. In 2008, the author's article "Treatment Progress Changes the Course of Alzheimer's Disease" published in the Shanghai Archives of Psychiatry, highlighted that at that time numerous drugs based on the AD pathophysiological hypothesis were in phase II of clinical trials.
The findings of several epidemiological studies revealed a considerable increase of the tau protein
and a decrease of the beta-amyloid level in the cerebrospinal fluid (6, 8).
Alzheimer's disease (AD) is a progressive degenerative disease of central nervous system and has two major characteristics including the formation of neurofibrillary tangles (NFTs) from the aggregates of excessively phosphorylated Tau protein
in neurons  and the formation of senile plaques (SPs) from the aggregates of [beta]-amyloid (A[beta]) outside neurons.
Like Alzheimer's disease, PSP belongs to the family of neurodegenerative disorders known as tauopathies; these diseases are associated with the formation and progressive spread of toxic oligomers of tau protein
in the brain.
The disease is characterized by degradation of brain tissue and the accumulation of tau protein
, causing symptoms such as memory loss, aggression, confusion and deep depression that generally appear years after initial brain trauma.