Graphical orientation disorder is a decrease in cognitive function of graphics, such as the inability to copy graphics, do structural work, connect the dots tests and arrange blocks and puzzles. About one in three people with Alzheimer’s disease will develop graphic orientation disorder. What are the causative factors of graphic orientation disorder? I. Genetic factors AD has family aggregation, about 20% of patients have positive family history and their first-degree relatives have a high risk of developing the disease. Molecular biology studies have demonstrated that there are abnormal loci on chromosomes 21, 19, 14 and 1. The proteins encoded by these affected genes are: beta-amyloid (beta-AP), apolipoprotein E (ApoE), progerin-1 (PS-1) and progerin-2 (PS-2). Mutations and polypeptide alterations in these genes are associated with AD pathogenesis. β-AP is produced by abnormal cleavage of β-amyloid precursor protein (β-APP) and is a major component of age spot formation. Apo E gene is one of the most important genetic factors affecting the aging pathway, and the risk of both late-onset familial AD and sporadic AD occurrence is associated with Apo E4 The risk of both late-onset familial AD and sporadic AD is dependent on the amount of the Apo E4 allele. II. Neurotransmitter theory The transmitter alterations associated with AD are acetylcholine system, monoamine system, amino acids and neuropeptide transmitters, among which the reduction of choline acetyltransferase and acetylcholine-type transmitters is an important cause of AD. Neuropharmacological studies have confirmed that patients with AD have reduced acetylcholine transferase activity in cortical and hippocampal sites, which directly affects the synthesis of acetylcholine and the function of the cholinergic system. In addition, growth inhibitory hormone, adrenocortical release factor and norepinephrine are significantly reduced in AD without patients, and dopamine hydroxylase activity is significantly reduced. Third, viral infection Experimentally, it was demonstrated that the virus that deformed the brain tissue of sheep inoculated into the brain of mice could appear typical age spots. In vitro experiments have shown that herpes virus infection can reduce the level of acetylcholine transferase in chromophobe PC12 cells. It is suggested that viral infection may be one of the causes of this disease. Fourth, the role of metal Some AD patients can reach 10-30 times the concentration of aluminum in the brain of normal brain, and aluminum deposition in the core of senile plaques (SP) and increased brain aluminum can be seen when dementia is caused by stealing, therefore, it is presumed that aluminum is related to dementia. However, it is not clear whether aluminum is the cause or the result of dementia. V. Immune dysfunction and free radical damage Immune dysfunction and free radical damage are associated with the development of AD. 20% higher brain reactive antibodies in AD than in controls, indicating that the increased autoantibody content in patients with this disease may play a role in the disappearance and aging of neurons.