الفهرس 
EpidemiologyOnly 14 pages are availabe for public view
 |  | from | 153 |  |  |
| | | from | 153 | | |
Abstract
Parkinson’s disease is a widespread neurodegenerative disorder, affecting up to 2% of
individuals over 65 and 10% of people over 80 years old. Besides motor dysfunction, cognitive
deficits have also been reported in PD patients. Clinical studies revealed mild cognitive deficits in
" ~ "30%-40% of newly diagnosed patients, and dementia in nearly 60%-80% of patients in the
advanced stage of the illness, which has a negative impact on their life expectancy, and everyday
functioning, and greatly impairs their quality of life.
The mechanisms underlying cognitive abnormalities in PD remain unclear and are usually
undiagnosed and, consequently, untreated. Numerous researchers believe that not only
neurochemical alterations in dopaminergic, cholinergic, and other systems but also
neuropathological contributions of limbic and cortical Lewy bodies and neurites, amyloid
deposition, NFTs, and even cerebrovascular disease, mitochondrial dysfunction, oxidative stress,
inflammation, autophagy dysfunction, and neurotrophic factors have frequently given rise to
cognitive deficits in PD.
Current pharmacotherapy is limited to symptom relief, particularly in the field of motor
symptoms. However, these drugs do not stop the progression of the disease and have incapacitating
side effects when used for an extended period of time. The lack of a meaningful treatment that can
be used after the disease is currently the main barrier to progress in the fight against Parkinsonism.
As a result, new PD strategies are required to prevent or slow the progression of motor and
cognitive symptoms.
Type 2 DM shares pathophysiological mechanisms with PD and neurodegenerative
dementias, such as central and peripheral insulin resistance, which leads to altered autophagy, cell
proliferation, and increased inflammation. As a result, evaluating the potential repurposing of
existing anti-diabetic drugs in the prevention of ROT-induced cognitive deficits in PD is of great
interest.
Sitagliptin, a drug that belongs to a group of medications that inhibits the DPP-4 enzyme,
PIO, a TZD derivative drug, which activates PPAR-γ receptors both are useful glucose-lowering
agents for patients with type 2 DM. These drugs have been explored by various researchers to treat
cognitive abnormalities linked to neurodegenerative disorders due to their neuroprotective effects,
including antioxidant, anti-inflammatory, antiapoptotic, autophagy-modulating, and neurotrophicsupporting
properties.