**Aging and Neurological Diseases**

Marta Kowalska, Michal Owecki, Michal Prendecki, Katarzyna Wize, Joanna Nowakowska, Wojciech Kozubski, Margarita Lianeri and Jolanta Dorszewska

Additional information is available at the end of the chapter

http://dx.doi.org/10.5772/intechopen.69499

#### **Abstract**

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62 Senescence - Physiology or Pathology

10.1016/j.cell.2007.02.022

Current knowledge indicates that the aging process starts with subclinical changes at the molecular level. These include the accumulation of mutations, telomere attrition, and epigenetic alterations leading to genomic instability. Such defects multiply exponentially over time, resembling a "snowball effect," and eventually leading to morphological and functional deterioration of the brain, including progressive neuronal loss, reduced levels of neurotransmitters, excessive inflammation, and disrupted integrity of vessels, followed by infarction and microbleeds. Additionally, the decreasing efficiency of DNA repair mechanisms increases the susceptibility to reactive oxygen species and spontaneous mutagenesis, resulting in age-related neoplasia. Moreover, the malnutrition and malabsorption seen commonly in the elderly may cause deficiency of vitamin B12 and folic acid, both necessary for homocysteine metabolism, and lead to vascular damage. Altogether, these lead to brain damage in old age and greatly increase the risk of developing diseases of the central nervous system, such as stroke, epilepsy, Parkinson's disease, Alzheimer's disease, and other dementias.

**Keywords:** aging, molecular factor, neurological diseases
