First, Alzheimer’s disease Alzheimer’s disease (AD) is a progressive degenerative disease of unknown etiology, is the most common cause of dementia, first described by Alzheimer (1907) in 1907, the incidence of AD increases with age, the prevalence rate of more than 65 years of age is about 5%, more than 85 years of age, 20%, the prevalence rate of males and females corrected for age is equal, and about 5% of the patients with AD have a definite About 5% of AD patients have a clear family history. Clinical manifestations include persistent progressive memory, language, visuospatial dysfunction and personality changes, etc. Mild amnesia of recent events and personality changes are the early symptoms of the disease, followed by a generalized decline in intelligent activities such as comprehension, judgment, and calculation. The clinical diagnosis of this disease includes: 1. According to the diagnostic criteria of dementia; 2. Emphasizing latent onset and progressive development; 3. Excluding all dementia caused by specific etiology. Generally after 5-10 years of development of severe dementia, until bedridden, and finally often due to bedsores, fractures, pneumonia and other complications or vital organ failure and death. Vascular dementia The age of onset of vascular dementia (VaD) is often between 50-60 years old. Vascular dementia, especially ischemic cerebrovascular disease, is the 2nd cause of dementia in adulthood, and the various morphological subtypes of VaD are: 1, small vessel infarct dementia, Binswanger, multiple lacunar states, and dementia due to multiple small cortical-subcortical infarct foci. 2, Dementia with multiple infarcts. 3, Critical site infarct dementia. Dementia with multiple infarcts is a common type of VaD. The pathogenesis of VaD is complex and is the result of multiple cerebrovascular diseases, and the occurrence of dementia varies according to the nature and location of the vascular lesions.The onset of VaD is generally more acute, and the symptoms of dementia usually become obvious after a stroke, and the course of the disease is aggravated in a step-like manner, and the impairment of cognitive function often fluctuates, and the intellectual impairment may only involve some limited cognitive functions, such as calculation, naming, etc. The patient’s personality may remain intact. The patient’s personality may remain intact, judgment may remain unimpaired for a long time, and a certain degree of self-awareness may be maintained. Some patients have severe anxiety and depression, and emotional disturbances in patients with overt dementia may be manifested by emotional lability and incontinence, emotional outbursts, and forceful crying and laughing. Most patients have neurologically localized signs, and the symptoms of dementia worsen with each stroke, with a stepwise progression of the disease. Binswanger’s disease is clinically characterized as a slowly progressive dementia with focal neurological impairment, and most patients have subacute progression of focal neurological impairment including walking impairment, pseudobulbar palsy, mild hemiparesis, ataxia, urinary incontinence, and asymmetric pyramidal symptoms. Brain CT and MRI show small lacunar lesions or large cerebral infarcts, multiple cerebral infarcts, etc. PET reveals localized metabolism and decreased blood flow in the infarct foci. In addition to the common neurological signs, the clinical manifestations of vascular dementia are difficult to distinguish from AD, and the diagnosis can be differentiated from AD according to the following clinical features: 1, often accompanied by hypertension and other parts of the atherosclerosis; 2, history of recurrent strokes or insufficient cerebral blood supply. 3, emotional instability and near-memory. Mood instability and near-memory impairment are the starting symptoms; 4. Personality and self-awareness are preserved for a longer period of time; 5. Intellectual decline occurs later; 6. The course of the disease is a stepwise progression alternating with jumps in exacerbation and incomplete remission; 7. Positive neurologic signs resulting from focal brain damage are often present. The survival period of vascular dementia is slightly higher than that of AD, and the treatment is mainly aimed at the primary disease. Generally, patients die of ischemic heart disease, serious cardiovascular accidents, renal failure, and sepsis within 5-6 years after the occurrence of dementia. Frontotemporal lobe dementia Frontotemporal lobe dementia is a dementia syndrome characterized by frontotemporal lobe atrophy, which is a common cause of neurodegenerative dementia, accounting for about 1/4 of all dementia patients. histopathological features are characterized by limited frontotemporal lobe atrophy, amygdala, hippocampus, substantia nigra, and basal ganglia can be affected, lack of neurogenic fibers tangle and amyloidosis characteristic of Alzheimer’s disease, and the clinical manifestations of invasive. The clinical manifestations of Alzheimer’s disease are insidious, slowly progressing, with personality and affective disorders in the early stage, such as irritability, anger, stubbornness, indifference and depression, etc., and behavioral abnormalities gradually appearing, such as inappropriate behavior, lack of aggressiveness, indifference and impulsivity towards things, excessive oral activity, gluttony, putting anything into the mouth to test, cognitive dysfunction, spatial orientation preservation, behavioral judgment ability and speech ability are obviously impaired, inability to think, few words, and poor vocabulary. , poor vocabulary, etc. Neurologic signs can be seen in the early stage of the disease, strong grip reflex, sucking reflex, and in the late stage of the disease, myoclonus, pyramidal fasciculations and Parkinson’s syndrome. Slowly progressive speech disorder without other cognitive dysfunction is the characteristic of this disease. Pick’s disease is a rare degenerative disease with unique pathological changes, about 20% of cases are familial autosomal inheritance, the pathological changes of frontal lobe and temporal lobe atrophy combined with some lobes of the brain obvious limited atrophy, symmetric enlargement of the ventricles, cerebral cortex severe atrophy, brain parenchyma atrophy, but the cerebellum is not affected, degeneration of the nerve cell cytosol is pear-like swelling, the body of Nystrom’s body disappears, there is lipochromatosis, the brain is not affected, and the brain is not affected. Nystrom’s body disappeared and there was lipid pigment deposition, which became Pick cells. With the development of the lesion, there were globular, homogeneous, well-bordered silver-loving stained inclusion bodies, i.e., Pick vesicles, in the plasma of the swollen neuronal cells. The disease is more common in females, and the prominent clinical manifestations are personality changes often occurring in the early stage, awkward behavior, reduced self-control, reckless sexual behavior or other indiscretions, reduced comprehension of the patient, and reduced ability to treat and socialize with others. As the disease aggravates, the patient’s intellectual impairment is gradually apparent, loss of interest in the environment, reduced speech, and speech disorders are an important feature of the disease, and a small number of patients can present with Focal cortical symptoms, such as blindness, dyslexia, dysgraphia, etc., in a longer period of time to maintain memory and time and place orientation, the definitive diagnosis of Pick’s disease depends on neuropathological examination. V. Lewy body dementia is a neurodegenerative disease characterized by fluctuating cognitive impairment, visual hallucinations and Parkinson’s syndrome, with Lewy bodies as the pathological feature, and the pathological feature is that there are Lewy bodies in the cytoplasm of neurons in the cerebral cortex and brainstem. It mostly develops in old age, and is rare in young and middle-aged patients. It mainly manifests three groups of symptoms, including progressive dementia, extrapyramidal movement disorders, and psychiatric disorders, and is characterized by fluctuating cognitive dysfunction, with insignificant memory impairment in the early stages, and aphasia, agnosia, and dysarthria may occur. The successive appearance of cognitive disorders and Parkinson’s symptoms within one year has diagnostic significance, and the psychiatric symptoms are characterized by shaped visual hallucinations, and myoclonus may occur, MRI scan shows temporal lobe atrophy is not obvious, which helps to differentiate from medial temporal lobe atrophy in AD. Progressive supranuclear palsy with extrapyramidal symptoms, similar to Parkinson’s disease, accompanied by limited upward and downward vision of both eyes, about 2/3 of the patients with dementia. Huntington’s disease, the age of onset of early AD, often middle-aged onset, clinically with involuntary dance-like movements as the main manifestation. Several years later, intellectual deterioration occurs simultaneously with or before the choreographic movements. Imaging examination shows atrophy of the cerebral cortex and caudate nucleus, and there is often a family history of autosomal dominant disease. Eight, normal cerebral pressure hydrocephalus typical symptoms of dementia, urinary incontinence and double lower limb gait instability, the cause of which are central nervous system infection, subarachnoid hemorrhage, traumatic brain injury or other unknown causes of cerebrospinal fluid circulation obstruction. Clinical dementia progresses faster, with normal cranial pressure, and brain CT or MRI shows obvious enlargement of cerebral ventricles without obvious atrophy of the cortex, which can be differentiated from AD. IX. Mild Cognitive Impairment (MCI) It is an age-inconsistent memory loss with basically normal overall cognitive function and normal daily living ability, which falls short of the diagnostic criteria for dementia. Patients with mild cognitive impairment whose neuropathology shows eventual progression to AD have brain neuropathologic changes similar to those of AD when clinical symptoms are not apparent. Patients may progress to frontotemporal lobe dementia, dementia with Lewy bodies, and AD later in life. Ten, Creutzfeldt-Jakob disease (CJD) Creutzfeldt-Jakob is a kind of central nervous system damage mainly prion disease, its clinical characteristics are mainly for the rapid progression of dementia, accompanied by multi-systems damage, short course, rapid progression, the mortality rate of 100%. It is a transmissible central nervous system disease characterized by rapidly progressive dementia and focal lesions of the cerebral cortex, basal ganglia, and spinal cord, and is a common human prion disease, also known as cortico-striatal-spinal cord degeneration. Pathologically, it is characterized by spongy changes in the brain, atrophic degeneration of the cortex, striatum and spinal cord, and loss of neurons under the microscope. Patients mostly have insidious onset of disease, slow progression, early manifestations of fatigue, inattention, insomnia, depression and memory loss, etc., but also headache, ataxia, etc.. In the middle stage, patients have progressive dementia, personality disorder, may be accompanied by aphasia, myoclonus, etc. Finally, patients have urinary incontinence, inactive muteness, coma and decorticate state, mostly due to pulmonary infection or decubitus ulcers and death. XI, AIDS caused by dementia acquired immunodeficiency syndrome, clinical manifestations of systemic failure and immune deficiency, causing a series of opportunistic infections, accompanied by a variety of mental disorders, HIV virus can be a direct invasion of the infected central nervous system, can also lead to opportunistic infections of the central nervous system, but also central nervous system tumors, cerebral vascular pathology and so on. Its dementia symptoms start insidiously, often with weakness, lethargy, lack of libido as the beginning, and later appear characteristic cognitive impairment, behavioral disorders, movement disorders, and in the late stage of reticence and urinary and fecal incontinence, but also can be combined with delirium and mental disorders, generally rapid progress, mostly in a few weeks and months to develop into severe dementia, and then death. Twelve, nutritional metabolic disorders of dementia, including vitamin B1 deficiency dementia, vitamin B12 deficiency dementia, folic acid deficiency dementia, serological examination shows that the corresponding blood concentration can be diagnosed. Dementia caused by physical diseases, including dementia caused by chronic respiratory failure, uremic encephalopathy, hepatic encephalopathy, hypothyroidism, can be diagnosed according to the patient’s history of the original disease. Toxic dementia can be caused by arsenic poisoning, mercury poisoning and barbiturates.