**1. Introduction**

Chlamydiae have been identified as viruses because they have a life cycle within the host cell and are smaller than bacteria. However, they were later classified as bacteria because they can also live outside the cell. With these conditions, they were named as "obligate intracellular bacteria" [1].

There are four species in the genus Chlamydia: *C. pecorum*, *C. psittaci*, *C. trachomatis* and *C. pneumoniae*. These species are classified according to their disease, antigenic structures, and intracellular inclusions. *C. pecorum* does not cause disease in humans. Others may cause disease in humans.

*C. trachomatis* is the most frequently sexually transmitted bacterium today [2]. It most commonly causes urethritis in men and cervicitis most commonly in women. If left untreated, it can progress to pelvic inflammatory disease in women. *C. trachomatis* is the most common cause of nongonococcal urethritis [3]. As a significant proportion of patients are asymptomatic, they continue to be contagious and act as vector [4].

This complicates the management of the disease and results in a serious socioeconomic burden, even in developed countries [5]. The three main clinical manifestations of urethritis—urethral discharge, itching, and dysuria—are mild or absent in some cases [6]. Therefore, diagnosing *C. trachomatis* infection is important. Although conventional diagnostic methods have low efficiency, PCR tests have high sensitivity and specificity and are currently the gold standard in the diagnosis of *C. trachomatis* infection. *C. trachomatis* can also cause ocular trachoma, lymphogranuloma venerum, and neonatal infections [7].

*Chlamydia Psittaci*; it causes a systemic disease that often progresses with pneumonia, being more common in occupational groups that come into contact with birds.

*C. pneumoniae*; it causes respiratory tract (such as pneumonia, bronchitis, sinusitis, and pharyngitis) infections and is also associated with atherosclerosis and cardiovascular diseases [8].

Chlamydia pneumonia is transmitted from person to person by direct respiratory route. The infection spreads slowly [9, 10]. It has a longer incubation period than many pathogens that cause respiratory tract disease, and this period is about a few weeks [11]. If it is within the family, the infection spreads in a shorter time [12].

Chlamydiae are obligate intracellular parasites and have a biphasic life cycle. They can grow and multiply using the host cell's ATP. Chlamydia are in the bacteria class because they are sensitive to antibiotics, reproduce by division, contain both DNA and RNA, and have cell membranes similar to gram-negative bacteria [13, 14].

Chlamydia reproduces by forming inclusion bodies in the cytoplasm of host cells. Chlamydia pneumonia has two forms called "Elementary body" (EB) and "Reticulate body" (RB). These two forms are functionally and morphologically different from each other and undergo regular change. The EB form is the metabolically inactive, extracellular form and causes contamination. It attaches to the mucosal surfaces of the respiratory tract by inhalation and enters the host cell by endocytosis, where it transforms into the RB form.

The RB form is metabolically active and utilizes the host cell's metabolism. It multiplies in the host cell, breaks up this cell, spreads around as newly formed elementary body bodies and continues to be transmitted. In its RB form, it is protected from the host cell's endocytic lysosomal digestive tract, where it can be stored for years. In this way, it causes a chronic inflammatory process in the body [15, 16].

Being located intracellularly provides the ability of this bacterium to transform into a resistant form [8, 17].

*C. pneumonia* lives in the host cell as a non-degradable inclusion separate from the cytoplasm of the cell. For this reason, it is protected from the host cell's defense systems by arranging the signal pathways used by the host cell for defense. In this way, *C. pneumoniae* cannot be eliminated because the host defense mechanisms are insufficient and may lead to persistent infection [18–20]. While *C. pneumoniae* lives in mononuclear cells, it multiplies from time to time and creates a chronic infection. In this chronic infection, heat shock protein ((HsP) and proinflammatory cytokine production takes place, and this process can initiate an autoimmunity process over time. As a result of chronic infection, *C. pneumonia* increases the expression of its own HsP60 proteins. The immune response of the host to microbial HsP60 is over time to human HsP60. This may contribute to the development of chronic diseases such as asthma, atherosclerosis, and coronary artery disease [11, 21, 22].

In recent years, there has been a great deal of information about the physiological effects of chlamydia infection on the host cell [23]. Although it is not known exactly how *C. pneumonia* may cause chronic infection in the central nervous system by affecting apoptotic pathways [24, 25].

In recent years, it has been determined that *C. pneumonia* may have a role in other chronic diseases in addition to respiratory tract diseases, as more powerful tests have been developed to show the presence of *C. pneumonia* [26].

It has also been shown to cause progressive diseases with chronic inflammation processes such as lung cancer, Alzheimer's disease, multiple sclerosis, arthritis, and atherosclerosis [18, 27–31].

The demonstration that various human cells (smooth muscle, monocytes, lymphocytes, macrophages, endothelium, and epithelium) are infected by *C. pneumonia* after a respiratory infection supports the systemic spread after respiratory tract infection [32]. Thus, *C. pneumonia* spreads everywhere through the circulatory system. Chlamydia, which invades the arterial wall as a result of endothelial damage, participates in the atherosclerosis process [33].

*Chlamydia* that invades the arterial wall as a result of endothelial dysfunction contributes to the atherosclerosis process [33]. However, *C. pneumoniae* infection has also been shown to promote monocytic migration via human brain endothelial cells, which is thought to be a mechanism by which the organism is able to enter the CNS. This mechanism may explain how the organism enters the CNS and causes chronic damage [34].

This chapter examines the potential role of chlamydial infections in different neurological diseases and the underlying mechanisms in light of the literature.
