The diagnosis of PSP still lacks biologically specific indicators. PSP should be considered in middle-aged and elderly patients with insidious onset and gradual onset of supranuclear gaze palsy with unstable gait, easy falls and tonic hypermobility. Specific diagnostic criteria are as follows: 1. Possible (Possible) PSP, required indicators: onset after 40 years of age, gradual progressive increase in ① vertical (upward or downward) supranuclear gaze palsy, or or ② slowing of upward and downward sweeping vision and significant gait disturbance with falls within 1 year of onset. One of ① and ② is present. There is no other disease that can explain the above symptoms. Indicators that must be excluded: recent history of encephalitis, limb agnosia, complex sensory deficits, localized frontal or temporoparietal atrophy and hallucinations and delusions unrelated to dopa therapy, Alzheimer’s type cortical dementia (severe memory loss, aphasia or dysarthria according to NINCDS-ADRA criteria). Supporting indicators: symmetrical hypermobility or tonicity, proximal heavier than distal, abnormal neck posture, especially in posterior extension, and Parkinsonian symptoms that are poorly or ineffectively treated with levodopa. According to this criterion clinical diagnosis of probable PSP its sensitivity is 83%, that is, 83% of cases at the first visit are clinically diagnosed as probable PSP. but its specificity is poor, the false-positive rate of up to 17%, suitable for descriptive epidemiological survey studies or clinical observation, even though there are some false-positive cases, but it includes almost all cases of PSP. 2, basic is (Probable) PSP necessary indicators: the onset of disease after 40 years of age, chronic progressive exacerbation. Vertical (upward or downward looking) supranuclear palsy and significant gait disturbance with falls within 1 year of onset. No other disease exists that would explain the above symptoms. Indicators that must be excluded: early onset of significant cerebellar signs or unexplained autonomic dysfunction (significant upright hypotension and dysuria), severe asymmetric Parkinson’s syndrome (e.g., decreased movement), neuroimaging evidence of associated structural disease (e.g., basal ganglia or brainstem infarction, lobar atrophy). Indicators of support: early onset of dysphagia and dysarthria. Early onset of cognitive impairment, including at least two of the following, affective apathy, abstract thinking impairment, poor verbal fluency, decreased utilization or imitation, and prefrontal release signs. The clinical diagnosis by this criterion is basically PSP with a specificity of 100%, but its sensitivity is only 50%, i.e. only half of the cases are diagnosed as likely PSP at the first visit. suitable for therapeutic, analytical epidemiological investigations and biological aspects of research. 3.Confirmed diagnosis is (definite) PSP, the necessary indicators: clinical diagnosis is likely to be or basically PSP, confirmed by histopathological examination in line with the typical pathological changes. Indicators that must be excluded: Whipple’s disease confirmed by PCR testing. Although clinical diagnostic indicators were identified, confirming the diagnosis still relies on neuropathological examination as the final basis posing certain difficulties in clinical practice. Therefore, the direction of future research is how to further improve the diagnostic accuracy of PSP using ancillary tests. A lot of work has been done in this area, such as neuropsychological studies of frontal lobe dysfunction; PET examination showing reduced glucose metabolism rate in frontal cortex and reduced striatal D2 receptor density; electrophysiological detection of auditory stimulus response test; analysis of early oculomotor disorder recordings and observation of fast eye movement sleep disorder using multilead sleep tracing technique, all of which are helpful for the diagnosis of PSP, but their specificity is not high. . Yagishita et al. conducted a retrospective study of the association between brainstem atrophy and signal alterations revealed by MRI scans and pathological change features in PSP patients, including MRI findings and brain specimens from 6 cases of PSP, 9 cases of PD, and 6 cases of striatal nigrostriatal degeneration (SND). Sagittal T1-weighted images showed shortened anterior and posterior midbrain diameters in 4 of the PSP patients, T2-weighted images showed high signal in the parietal and perineural caps of the midbrain in 4 cases, and high signal in the superior and inferior pontine caps of the brain in 4 cases, and the sites of these signal changes were consistent with pathological changes, whereas no similar changes were seen in the PD and SND patients. It is believed that midbrain atrophy and diffuse high signal in the T2-weighted images of the periaqueductal and parietal lobes of the brainstem are characteristic changes of PSP MRI. The author believes that the study of the chemical composition of the NFT as well as the linear reticular formation characteristic of PSP pathology to clarify its composition as well as the mechanism of gene expression and to identify the specific components of it, while as a specific diagnostic marker for peripheral body fluid examination may be helpful for the early diagnosis of PSP.