**1. Introduction**

Physiological aging starts after 60 years of age. Senescence in both animal models and humans is accompanied by alterations in the function of central cholinergic neurons. These changes essentially involve decreased levels of cholinergic receptors, reduced synthesis and release of acetylcholine, and a marked decrease in the number of muscarinic cholinergic neurons, all which may be linked to the age-related memory deficits, a typical change in

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**Figure 1.** Molecular factors associated with aging and age-related neurological diseases. The pathological changes starting at the molecular level induce oxidative stress and disturb cell cycle that affects cells of the aging organism and lead to systemic deterioration. The genetic variation may give rise to age-related neurological diseases. ROS reactive oxygen species, HHcy—hyperhomocysteinemia, AEDs—antiepileptic drugs, AD—Alzheimer's disease, and PD—Parkinson's disease.

Alzheimer's disease (AD) patients. Moreover, a decrease in the levels of dopaminergic neurons of up to 40–50% may be observed in the *substantia nigra* and of dopamine in the striatum at the end of the sixth decade of life, which are typical changes seen in patients with Parkinson's disease (PD).

Increased longevity in much of the developed world appears to have lead to higher stroke incidence. Apart from an aging population, there is a significant impact of the growing prevalence of hypertension, diabetes, obesity, and disorders of the cardiovascular system on the increase in the incidence of stroke. The prevalence of these diseases increases with age.

The most common causes of epilepsy in the elderly are vascular changes in the brain (approximately 5%) and degenerative diseases of the central nervous system (CNS) (10–20%). Seizures also occur in patients with AD, demyelinating diseases (multiple sclerosis, or MS), metabolic disorders, as well as in toxic and hormonal disorders, or in individuals with a history of brain injuries or CNS infection.

The mechanisms leading to the development of neurological disorders in the elderly have not been fully elucidated. There are no known mechanisms that regulate cell death in the aging brain. It is not known whether the age of various cells induces the process of apoptosis and other mechanisms of neuronal death, and what factors determine the susceptibility to developing neurological diseases in old age. Understanding the causes of the increased incidence of neurological diseases in the elderly may help in their prevention and improve quality of life in old age (**Figure 1**).

The following review is based on literature search through public databases, such as PubMed and Scopus, with the use of keywords: "aging," "molecular mechanism," "neurological diseases," "stroke," "epilepsy," "vascular dementia," "Alzheimer's disease," "Parkinson's disease," and "brain tumor." Subsequently, the authors selected eligible publications and performed further searches through their references in order to find additional articles. The last search was performed in February 2017.
