Health benefits of Custard Apple ,Nutrtion Bioactivities

 

. 2025 Oct 2;14(19):3413. doi: 10.3390/foods14193413

A Review of Nutrition, Bioactivities, and Health Benefits of Custard Apple (Annona squamosa): From Phytochemicals to Potential Application

Ningli Qi ^1,2, Xiao Gong ^1,2,*, Yang Luo ³, Chenghan Zhang ⁴, Jingjing Chen ^1,*, Tinghui Chen ²

Editors: Antonio Cilla, Rafael Guillén Bejara

Abstract

The custard apple (CA) is a noble fruit in tropical regions inworldwide. It has attracted a growing interest due to its organoleptic properties and nutritional value.

 With the expansion of international trade, both its cultivation and consumption have grown significantly in recent years. Previous researchers have sporadically investigated its nutritional composition and health benefits; however, existing information on its processing and utilization is highly fragmented and lacks a comprehensive overview of its constituents, biological activities, and potential applications. 

This review is a detailed summary of the nutritional and bioactive properties, safety evaluations, and potential applications of CA. Following PRISMA guidelines, peer-reviewed studies published between 2000 and 2025 were systematically searched in PubMed, Scopus, ResearchGate, and Web of Science. Inclusion criteria comprised studies reporting on nutritional composition, phytochemicals, bioactivities, health promotion, and applications of CA.

 In addition to primary nutrients like carbohydrates, protein, fatty acids, vitamins, and minerals, 

CA also contains a multitude of bioactive compounds, mainly including phenols, flavonoids, terpenoids, acetogenins, and alkaloids, which are attributed to a range of health benefits,

 such as antioxidant, anti-microbial, anti-tumor, blood sugar regulation, and cognitive function improvement.

 However, more clinical and toxicological profiles remain underexplored, and future research should focus on standardized extraction, safety evaluation, and translational applications. Additionally, the challenges and future perspectives in industrial applications are discussed, which are expected to offer comprehensive information for the utilization of CA.

  Thesis References Path 

1 Pub med

2Books

3 cross references 

4 Read the cross references care fully

With minimum time it's skill the title of reference will help you to

judge if it could help you.

5 keep a xcell record of each references how old is journal

When the first article was published.

6 pub med helps you to know eta when your reference was studied

Extensively

 Lastly write comments 

This is second article

How to write for Ph D thesis?

 How to write PhD Thesis?

Mostly student write  after completing research work.

This requires lot of time to finish writing 

The solution is 

Following tips

1 as soon as guide sends tile of thesis topic to University 

Start writing

2 Start writing Reviewof literature

As you know it is continuous process 

Library reading is required

Try to read full length article underline important lines key points.

3 This will save lot of time will help your presentation style

During conference.

4write material andmethods as you progress

5 Results description is on going process. Write

After experiment .

6 Discussion is most difficult chapter

Guide may not accept what you write as it is not result part

But the way your results different from previous what are new

findings.

Crow is the Pilot

   Yes, the crow is a pilot, 

a passenger, a control tower

He does the work of the  control tower

No need for a black box, no petrol, but fuel is needed

Yesterday I. First the crow was eating a piece of bread and then

Pilot 

He planned where to fly

The food he eats is his food for his stomach and

And petrol is fuel.

How accurate is his vision? Flying in a moment

How difficult is life

How much energy does he get by eating?

How small is his brain but he has the strength to 

do the above tasks

Between a crow and a beggar, a crow is very good because he

Calls other friends with the food he gets

कावळा एक पायलट

 हो कावळा एक पायलट आहेत प्रवासी आहे कंट्रोल

 टॉवर चे काम तोच करतो

ब्लॅक बॉक्स ची गरज नाही पेट्रोल नाही पण इंधन लागते

कालच मी. पहिले कावळा कुरमुरे  वेचुन  खात होता आणि नंतर 

 पायलट महाशय

उडाले कुठे जायचे ते  प्लान स्वतः कडे 

खाण्यात त्याच्या आलेले अन्न हेच त्याच्या पोटासाठी पोटपणी आणि 

आणि पेट्रोल समान इंधन.

किती अचूक दृष्टी धोके दिसता क्षणात उडणे 

खरच किती अवघड जीवन

किती खाऊन उडण्याची ऊर्जा येत असेल ?

मेंदू किती छोटा पण वरील कामे करण्यास ताकद असणारा

कावळा आणि भिकारी यात कावळा हा खूप चांगला कारण तो

मिळालेले खाद्य इतर दोस्तांना बोलावून देणारा

इडली मार्केटिंग

 हो इडली मार्केटिंग केली जाते

काही वर्षे झाली अंदाजे  50 वर्षाहून अधिक काळ

मार्केटिंग स्टाईल आगळी वेगळी होती

कोणी इडली घेता का? आरोग्यास चांगली

अशा घोषणा नाहीत

रस्ताने हे विक्रेते फिरत पण तोंडाला आराम देऊन विक्री चांगली होत असे आज ही होते

काही एक रबराचा हॉर्न वाजवून तो ही हाताने तोंडाला आराम  ग्राहक बोलावी ते ठराविक आवाज आल्या. वर नवीन पोजिशन केली आज ही पध्दत आहे.

पाव  वाला पाव पाव आवाज देतो सायकल ने फिरतो

धार वाला धार् वाला म्हणतो

जूने समान वाला समान जून पुराणे घेतो असा आवाज देतो

आवाज ही गरज आहे ती बासरी विकणाऱ्याला  बासरी घेऊन

तीच बासरी ते गण आपण नाही गाऊ शकत

Effect of Air Pollution and Neurological Dsease

 

Ref

Front Public Health. 2022 Jul 14;10:882569. doi: 10.3389/fpubh.2022.882569

The Physiological Effects of Air Pollution: 

Particulate Matter,

 Physiology and Disease

Jack T Pryor 1,2, Lachlan O Cowley 1, Stephanie E Simonds 1,*

Abstract

Nine out of 10 people breathe air that does not meet World Health Organization pollution limits. 

Air pollutants include gasses and particulate matter and collectively are responsible for ~8 million annual deaths.

 Particulate matter is the most dangerous form of air pollution, 

causing inflammatory and oxidative tissue damage. 

A deeper understanding of the physiological effects of particulate matter is needed for effective disease prevention and treatment.

 This review will summarize the impact of particulate matter on physiological systems, and where possible will refer to apposite epidemiological and toxicological studies. By discussing a broad cross-section of available data, 

we hope this review appeals to a wide readership and provides some insight on the impacts of particulate matter on human health.

Particulate Matter

Particulate matter (PM) are solid compounds suspended in air that are sufficiently small to be inhaled (Figure 1)

. PM is categorized by particle diameter (measured in μm); PM0.1, PM2.5 and PM10 whilst 

ambient concentration is usually quantified as μg/m3.

 Some PM are of natural origin (bushfires, dust, sea spray, aerosols, etc.) but anthropogenic PM (diesel, coal and biomass combustion and emissions from metal refineries etc.) are the most dangerous to health (13).

 High atmospheric concentrations of human-made PM, and toxic and oxidative chemical characteristics render them disproportionately hazardous (13).

 Elemental and complex chemical species of PM are diverse, with surface shape, chemistry and charge impacted by emission source and environmental conditions. PM chemistry can change through reactions with other airborne PM and be affected by the oxidative effects of ozone and low ambient pH (14, 15).

Fig 1

To scale illustration of the relative sizes of PM10, PM2.5, and PM0.1. Representative macrophage and mitochondria are included to scale for

Reference

Fig1

Neurological Disease

Increased ambient PM concentration positively correlates with the incidence of Alzheimer's disease, Parkinson's disease, Multiple Sclerosis, dementia and autism spectrum disorder (Figure 2) (127)

. Long-term PM2.5 exposure significantly increased age adjusted risk of mortality and hospital admission for Alzheimer's disease, Parkinson's disease and non-Alzheimer's disease dementia (128). 

This study found the strongest correlation to exist between PM2.5 and Alzheimer's disease (128). One longitudinal study found that people living within 50 meters of a main road had a 12% greater chance of dementia diagnosis (129).

 PM2.5 exposure is linked to faster decline in new learning and immediate recall, as well as MRI-detected gray matter atrophy in brain areas vulnerable to Alzheimer's disease pathology (130).

 PM2.5 exposure has been linked to Alzheimer's specific cognitive impairments (CERAD score but not ABC score) however post-mortem analysis of neuropathology in the brains of Alzheimer's disease patients failed to reveal any link between PM2.5 exposure 10 years before death, and disease progression indicated by Braak stage (131)

. The impact of specific PM (including black carbon, organic matter, nitrate, sulfate, sea salt and soil) exposure on the rate of initial Parkinson's disease hospitalization in New York State was investigated. This study revealed that with each standard deviation increase in either nitrate or organic matter PM, the risk of hospitalizations increased 1.06-fold (132).

PM 0.1 can cross the blood brain barrier and cause inflammatory and oxidative tissue damage as well as microglial activation (133). 

Glutamatergic excitotoxicity is a common reported endpoint for acute PM induced pathophysiology in the central nervous system. PM has been found in neurons, glia, endothelium, choroid plexus ependymal cells, cerebrospinal fluid, nasal epithelium, and olfactory epithelium of individuals subjected to PM exposure (134).

 PM2.5 has been found to reduce nervous system expression of the tight junction proteins, zonula occludens 1 and 2 (135). 

This study found a compromised blood brain barrier permeable to macrophage infiltration, and nervous system tissue subject to glutamatergic excitotoxicity, triggered by macrophage-derived glutamate (135).

 In mice, PM2.5 has been shown to reach the olfactory bulb and induce microglial activation and glutamatergic excitotoxicity that could be blocked with the antioxidant N-acetylcysteine (136).

Alzheimer's disease is characterized by cortical and hippocampal amyloid-β plaque and tau tangle deposition. Amyloid-β plaque formation and gliosis underlie at least some of the cognitive deficits associated with 

AD progression (137).

 In a transgenic mouse model of Alzheimer's disease, exposure to diesel emission PM2.5 exacerbated amyloid-β plaque deposition, and increased astrocytosis and microgliosis. Additionally, elevated inflammatory cytokines including tumor necrosis factor, nuclear factor-α, interleukins 1β and 6, interferon-γ and macrophage inflammatory protein-3α were identified in the cortices of double transgenic mice (138).

 In a similar study, 13-week exposure to diesel exhaust PM also accelerated cortical amyloid-β plaque deposition, an effect associated with significant impairments to motor coordination (139). Parkinson's disease is caused by loss of dopaminergic neurons in the substantia nigra of the basal ganglia. Neuron loss results in diminished cortical input and associated behavioral and cognitive deficits. In a rotenone-induced mouse model of Parkinson's disease, PM2.5 exposure induced mitochondrial dysfunction, oxidative stress and apoptosis in the substantia nigra. In the same study, PM exposure also exacerbated motor and somatosensory deficits (140). 

Multiple Sclerosis (MS) is a progressive, demyelinating and neurodegenerative disease of the CNS. Short-term PM exposure is associated with increased MS hospital admissions and relapse (127). In a mouse model of lipophosphatidylcholine-induced demyelination, PM exposure impairs myelin repair and sustains astroglia and microglia dependent neuroinflammation. PM2.5 exposure to rats impaired spatial learning and memory, inquiring ability and sensory function, these changes were related to ultrastructural changes to mitochondria and myelin (141).

 Mice exposed to PM2.5 for 10 months developed structural hippocampal alterations including diminished apical spine density and dendritic branching of hippocampal neurons and behavioral studies revealed reduced spatial learning and memory impairments (142).