Ahidjo Nene, Seke Etet Paul F, Ngarka Leonard, Maidawa Yaya Frederic, Ndianteng Ethel W, Eyenga Nna Aude L, Meka'a Zang Luc Yvan, Kemmo Christelle, Nwasike Caroline N C, Yonkeu Tatchou Floriane G, Njamnshi Wepnyu Y, Nfor Leonard N, Tsouh Fokou Patrick V, Djiogue Sefirin, Fekam Boyom Fabrice, Ngadjui Bonaventure T, Njamnshi Alfred K
Brain Research Africa Initiative (BRAIN), P.O. Box 25625, Yaoundé, Cameroon.
Neuroscience Laboratory, Faculty of Medicine and Biomedical Sciences, The University of Yaoundé I, P.O. Box 25625, Yaoundé, Cameroon.
Brain Commun. 2024 Dec 31;7(1):fcae441. doi: 10.1093/braincomms/fcae441. eCollection 2025.
Epidemiological evidence associates latent infection with the development of neuropsychiatric disorders, and various immunological and environmental factors play key pathophysiological roles through host immune response alterations. We investigated the cognitive and motor alterations occurring in the terminal stage of infection in rats, and whether a low-protein diet, a high-fat diet or ovariectomy may accelerate their development, given the role of malnutrition and menopause on immunity and resistance to infection. In two sets of experiments, 2-month-old (157.5 ± 4.3 g, = 42) male ( = 18) and female ( = 24) Wistar rats were infected with (ATCC 40050). Open-field and elevated plus maze tests were performed in the terminal stage of infection first and then in the early stage in low-protein diet-fed, high-fat diet-fed and ovariectomized infected rats. Late-stage (90 days) infected and early-stage (17 days) low-protein diet-fed groups showed significant decreases in body weight (42.42%↓, = 0.016 and 57.14%↓, < 0.001 versus non-infected, respectively), increases in body temperature ( = 0.001 and < 0.001, respectively), decreases in blood glucose levels ( = 0.006 and = 0.020, respectively), signs of cognitive and motor impairment and lower neuron counts. The alterations observed in high-fat diet-fed and ovariectomized infected animals were milder. Low-protein diet feeding to -infected rats accelerated the occurrence of the infection terminal stage. Thus, a diet low in proteins could transform a slow early-stage infection into an active neurotoxoplasmosis with neuropsychiatric manifestations and possible neurodegeneration in rats.
流行病学证据表明潜伏感染与神经精神疾病的发生有关，各种免疫和环境因素通过改变宿主免疫反应发挥关键的病理生理作用。鉴于营养不良和绝经对免疫及抗感染能力的影响，我们研究了大鼠感染末期出现的认知和运动改变，以及低蛋白饮食、高脂饮食或卵巢切除术是否会加速这些改变的发生。在两组实验中，将2月龄（157.5±4.3 g，n = 42）的雄性（n = 18）和雌性（n = 24）Wistar大鼠感染刚地弓形虫（ATCC 40050）。首先在感染末期对感染大鼠进行旷场试验和高架十字迷宫试验，然后对低蛋白饮食喂养、高脂饮食喂养和去卵巢的感染大鼠在早期进行同样的试验。感染后期（90天）和低蛋白饮食喂养早期（17天）的组体重显著下降（分别下降42.42%，P = 0.016和57.14%，P < 0.001，与未感染组相比），体温升高（分别为P = 0.001和P < 0.001），血糖水平降低（分别为P = 0.006和P = 0.020），出现认知和运动障碍体征以及神经元数量减少。在高脂饮食喂养和去卵巢的感染动物中观察到的改变较轻。对感染刚地弓形虫的大鼠进行低蛋白饮食喂养加速了感染末期的出现。因此，低蛋白饮食可能会将大鼠早期缓慢的弓形虫感染转变为具有神经精神表现及可能神经退行性变的活动性神经型弓形虫病。
