Alzheimer's disease (AD) is the most common form of dementia. Several hypotheses have been put forward to explain the basis of disease onset and progression. A complicated array of molecular events has been implicated in the pathogenesis of AD. It is attributed to a variety of pathological conditions that share similar critical processes, such as oxidative stress, proteinaceous aggregations, mitochondrial dysfunctions and energy failure. There is increasing evidence suggesting that metal homeostasis is dysregulated in the pathology of AD. Biometals play an important role in the normal body functioning but AD may be mediated or triggered by disproportion of metal ions leading to changes in critical biological systems and initiating a cascade of events finally leading to neurodegeneration and cell death. The link is multifactorial, and although the source of the shift in oxidative homeostasis is still unclear, current evidence points to changes in the balance of redox transition metals, especially iron, copper (Cu) and other trace metals. Their levels in the brain are found to be elevated in AD. In other neurodegenerative disorders, Cu, zinc, aluminum and manganese are involved. This paper is a review of recent advances of the role of metals in the pathogenesis and pathophysiology of AD and related neurodegenerative diseases.
The effects of different estrus synchronization techniques on follicular development and estrus response were studied in 81 nulliparous Boer does. The does were divided into nine groups. Eight of the nine groups were synchronized with prostaglandin F2-alpha (PGF(2α)) or flugestone acetate (FGA) or their combinations, and the ninth group was a control group. In addition to the above combinations, four of the eight synchronized groups were given 5 mg follicle-stimulating hormone (FSH) and the remaining four groups were administered 300 IU equine chorionic gonadotrophin (eCG). Posttreatment follicular development was monitored until ovulation occurred using a real-time B-mode ultrasound scanner (Aloka, 500 SSD, Japan), with a 7.5-MHz transrectal linear probe. All the does from the synchronized groups that were given eCG exhibited oestrus while only 88.9% of the does synchronized with FSH showed estrus. The estrus response was observed to be the least among the does synchronized with PGF(2α) + FSH (33.3%) combination followed closely by the FGA + FSH (42.9%) combinations. It was observed that the combinations of FGA + PGF(2α) + FSH resulted in increased percentage of estrus response, duration of estrus, and ovulation. The number of follicles was higher (P < 0.05) in FSH-synchronized groups than the eCG-synchronized groups. It was concluded that the best estrus synchronization protocol in goats is the FGA + eCG with or without PGF(2α). However, the PGF(2α) + FGA + FSH method of estrus synchronization is the most promising combination for further development as a better alternative to estrus synchronization with eCG in does.
The effects of estrus synchronization with prostaglandin F(2α) (PGF(2α)) and Controlled Internal Drug Release Device (CIDR) on ensuing antral follicular development were documented and compared to natural estrous cycles of non-seasonal tropical goats. Two to six follicular waves were observed, with the three-follicular wave pattern being most frequently observed (58%), followed by four follicular waves (31.6%) per estrous cycle. There were no significant differences (p>0.05) between the PGF(2α)- or CIDR-synchronized and natural estrous cycles nor between the synchronized and subsequent non-synchronized cycles in terms of the time of ovulation, the duration of inter-ovulatory intervals, daily numbers of antral follicles ≥3mm in diameter, and the number of follicular waves per cycle in the goats of the present study.