Effect of phosphatidylserine on memory in patients and rats with Alzheimer’s disease

Abstract

ABSTRACT. The aim of this study was to investigate the effect of phosphatidylserine (PS) on memory of patients and rats with Alzheimer's disease (AD). In total, 57 AD patients were recruited from our hospital, and were divided into two groups: 25 in the control group and 32 in the observation group. Next, 300 mg/d of PS was given to the rats in the observation group for 12 continuous weeks based on the control group. AD rats were divided into three groups: control group, PS 30 mg/kg group, and PS 15 mg/kg group. Learning memory ability and free radical levels in the brain were detected after treatment. In AD patients, vocabulary and picture matching scores in the two treatment groups increased after treatment (P < 0.05). Moreover, the scores in the treated group were significantly greater than the control group (P < 0.05). In AD rats, PS treatment reduced the escape latent period of AD rats, increased SOD and OH -, and decreased acetylcholinesterase levels (P < 0.05). Compared with PS 15 mg/kg, PS 30 mg/kg group was significantly more efficacious (P < 0.05). Compared with the AD model group, hippocampal cells showed normal arrangement, karyopyknosis decreased, and the pathological changes in the two PS groups were considerable. In conclusion, PS decreased cholinesterase, improved memory, and improved hippocampal inflammation injury in AD brains by increasing SOD and OH -levels.

Phosphatidylserine Ameliorates Neurodegenerative Symptoms and Enhances Axonal Transport in a Mouse Model of Familial Dysautonomia

“…The responses to treatment with broad-spectrum HDAC inhibitors are heterogeneous, protective in some cases and detrimental in others [95]. Recently PS treatment has been reported to improve memory in Alzheimer’s patients and to reduce hippocampal inflammation and free radical production in a rat model of Alzheimer’s disease [96]. The fact that PS has been used clinically with no serious side effects and promotes neuron survival and axonal transport suggest that PS might be relevant as treatment for other neurodegenerative diseases that share similar pathologic and molecular mechanisms.…”

The Additive Effects of Low Dose Intake of Ferulic Acid, Phosphatidylserine and Curcumin, Not Alone, Improve Cognitive Function in APPswe/PS1dE9 Transgenic Mice

“…This increasing effect on acetylcholine was believed to be due to PS, as reported previously. [22][23][24] However, we did not observe any increase in acetylcholine in the Cur group (Fig. 4K).…”

“…Some kinds of phospholipids, such as phosphatidylcholine (PC; also called lecithin) or plasmalogens other than PS, also seem effective in preventing and treating AD. PC, like PS, [22][23][24]122) is an important factor that makes up the nerve cell membrane and also a source of acetylcholine. 123,124) PC is found to decrease in an AD patient's brain, 99) so replenishment of PC is expected to prevent and treat AD.…”

“…Studies have reported that PS administration improves these conditions, in addition to cognitive function. 20,21) PS also promotes acetylcholine release, [22][23][24] decreases the acetylcholinesterase (AChE) level, 25) maintains N-methyl-D-aspartate (NMDA) receptor, 26) and contributes to Aβ clearance through exosome secretion. 27) Curcumin (Cur; Fig.…”

Glycerophospholipid Supplementation as a Potential Intervention for Supporting Cerebral Structure in Older Adults

“…The consumption of phospholipids (PL) and in particular the glycerophospholipids (GPL), may also benefit cerebral structure and subsequently cognitive function in older adults. The GPL species phosphatidylcholine (PC), phosphatidylethanolamine (PE), and phosphatidylserine (PS) are abundant in mammalian cell membranes, and there is growing evidence that provision of these GPL (particularly PC and PS) can improve cognitive function in animals via oral supplementation (Zanotti et al, 1989 ; Furushiro et al, 1997 ; Lim and Suzuki, 2000 ; Suzuki et al, 2001 ; Kataoka-kato et al, 2005 ; Yaguchi et al, 2009 , 2010 ; Lee et al, 2010 ; Babenko and Semenova, 2011 ; Nagata et al, 2011 ; Park et al, 2013 ; Zhang et al, 2015 ; Qu et al, 2016 ; Wen et al, 2016a , b ) or intraperitoneal/intracerebral injection (Drago et al, 1981 ; Zanotti et al, 1984 ; Corwin et al, 1985 ; Sakai et al, 1996 ; Blokland et al, 1999 ; Claro et al, 1999 , 2006 ; Suzuki et al, 2000 ). Similar results are also evident following oral supplementation in older humans with varying levels of cognitive function (i.e., normal cognitive function with subjective memory complaints, age-related “cognitive dysfunction,” AAMI, MCI, or dementia).…”