Parkinson’s disease (PD), the second most common neurodegenerative disorder after Alzheimer’s disease (AD), is characterized by motor and behavioral disturbances that include a resting tremor, postural instability and bradykinesia . PD affects approximately 2% of the population, although incidence varies across age, gender and race .
PD is often complicated by a variety of cognitive symptoms that range from isolated memory and thinking problems to severe dementia. While the motor symptoms of PD are well-known (tremor, rigidity, slowness of movement, imbalance), the commonly seen deficits in memory, attention, problem-solving, and language are less understood. Studies have shown that over 50% of people with PD experience some form of cognitive impairment. About 20% have more substantial cognitive impairment . Memory problems in PD are typically milder than in Alzheimer’s disease. In PD, the person may have difficulty concentrating, learning new information and recalling names . Non-motor symptoms in advanced stages of PD such as depression, dementia, sleep abnormalities and autonomic failure are probably the consequence of degeneration of both dopaminergic and non-dopaminergic systems, which still lacks efficacious treatments at present .
Although the etiology of the neurodegenerative processes found in PD is not completely understood, it is suggested that a state of oxidative imbalance is triggered by one or more factors, among which are brain aging, genetic predisposition, mitochondrial dysfunction, free radical production and environmental toxins [5–8].
Neuropathological evidence from both human and experimental models of PD firmly supports a significant role for oxidative stress in the death of dopaminergic (DA) neurons in the substantia nigra (SN) . Although no model to date has been able to recapitulate all the pathological features of PD, the genetic or neurotoxic animal models of PD have contributed much to our understanding of human PD [10, 11]. Neurotoxins-based models of PD have a long history and represent the most important models while genetic animal models have failed to recapitulate the key neurobehavioral or pathological features of PD [10, 11].
6-hydroxydopamine (6-OHDA), 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) and rotenone, are the most successful agents so far to mimic parkinsonism in vitro and in vivo. 6-OHDA is taken up by the dopamine transporter (DAT) and it then generates free radicals . Extensive study of these models has defined important cellular actors of cell death including oxidative stress, mitochondrial dysfunction, excitotoxicity, neuroinflammation and nitric oxide which is presumably critical of the nigral degeneration [13, 14]. Furthermore, the neurotoxic models can serve as valuable tools for the assessment of efficacy and side-effects of symptomatic treatments of PD and have offered a basis for the development of novel therapeutic strategies .
Discovery of new drugs from traditional medicine is not a new phenomenon. Current researches are focusing on finding therapies, preferentially from natural products which could help in preventing/delaying the ongoing neurodegeneration in PD [16, 17]. Research confirms that several medicinal herbs-based extracts increase redox/antioxidative abilities of the body and can effectively slow the progression of PD [3, 17, 18].
Among the plants used in traditional medicine, Albizia adianthifolia (Schumach.) W. Wright (Fabaceae) is commonly used in Cameroon as a remedy. In fact, it grows in most African countries. Its use in traditional medicine varies from one country to another. The sap is applied on the eye to treat river blindness and conjunctivitis, used as decoction, leaves treat respiratory diseases and have analgesic proprieties. An infusion or decoction of the bark is used to treat scabies and other skin diseases. A decoction of the leaves is administered as a purgative, as an analgesic and against inflammation. In Central and West Africa, this plant is used for the treatment of skin diseases, bronchitis, tapeworm, headaches and sinusitis [19, 20].
Aqueous and ethanol extracts of A. adianthifolia (Schumach.) W. Wright (stem bark) used in southern Africa to treat memory loss and Alzheimer’s disease, have been screened for acetylcholinesterase inhibitory activity . The root ethanolic extract of this plant showed in vitro immunomodulatory activity on the Jurkart T cell . Kim et al.  reported that the aqueous extract of A. julibrissin had anxiolytic-like effects in rats as assessed using the elevated plus-maze test. Also, a recent study indicated that julibroside C1 extracted from A. julibrissin stem bark produced potent anxiolytic-like effects in mice . Aurantiamide acetate was the most active compound isolated from the stem bark of A. adianthifolia through antioxidant activity (DPPH) and trolox equivalent antioxidant capacity (TEAC) assays were used to detect the antioxidant activity EC50 values 9.51 μg/ml and 78.81 μg/ml, respectively. The bark extracts of A. lebbeck possess free radical scavenging activity against 1,1-diphenyl-2-picrylhydrazyl radical (DPPH) and reducing power assays. Their results on DPPH free radical scavenging at 1000 μg/ml indicated maximum antioxidant activity of 91.82% and 90.08%, respectively. Ethanolic extract of A. procera showed strong scavenging activity against free radicals compared to various standards. These in-vitro assays indicate that these plant extracts are a good source of natural antioxidants, which might be helpful in preventing the progress of various oxidative stresses , with relevance for Parkinson’s disease conditions.
Despite extensive knowledge about the effects of Albizia species extracts, there is no study clarifying the possible cognitive-enhancing and antioxidant potentials of A. adianthifolia leaves extract in animal models of PD.
In this way, the present study aims to investigate the possible antioxidant activity and behavioral recovery following chronic administration of the aqueous extract of A. adianthifolia leaves using a unilateral 6-OHDA-lesion rat model of PD.