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Vol 1 | Issue 1 | Apr – Jun 2022                                                                                     Indian J Pharm Drug Studies | 10  

Review Article  

The Link between Cholesterol and a Brain Disease       

Sujeetha Purushothaman1, Arumugan Vijaya Anand1  

From, 1Medical Genetics and Epigenetics Laboratory, Department of Human Genetics and Molecular Biology, Bharathiar University, 

Coimbatore, Tamil Nadu, India.  

Correspondence to: Sujeetha Purushothaman, Medical Genetics and Epigenetics Laboratory, Department of Human Genetics and 

Molecular Biology, Bharathiar University, Coimbatore - 641046. Tamil Nadu, India. Email: suji648@yahoo.co.in 

ABSTRACT 

Lipids comprise the immensity dry mass of the brain and these have been allied with healthy function as well as the most common 

pathological circumstances of the brain. Genetics and lifestyles are the most important factor that influences the lipid metabolism and 

the key components of lipid disruption in Alzheimer’s disease (AD). Additionally, the most common genetic risk factor of AD, APOE 

E4 genotype, is involved in lipid transport and metabolism. Under healthy conditions, lipid homeostasis bestows a balanced cellular 

environment that enables the proper functioning of brain cells. However, under pathological conditions, dyshomeostasis of brain lipid 

can result in disturbed BBB, abnormal processing of APP, dysfunction in endocytosis/exocytose/autophagocytos is, altered myelination, 

disturbed signaling, unbalanced energy metabolism, and enhanced inflammation. This lipid instability may contribute to abnormalities 

in brain function that are the hallmark of AD. In this Review, we focus on the lipid and cholesterol metabolism, with an overview of 

the various lipid and cholesterol metabolic pathways and changes that have been linked to AD.  

Key words: Alzheimer’s disease, Lipid homeostasis, Inflammation, Apolipoprotein E

eregulated lipid and cholesterol homeostasis in the 

body and particularly in the brain has been 

demonstrated in neurodegenerative diseases such as 

Alzheimer’s disease (AD), as well as Parkinson’s 

disease (PD) and Huntington’s disease (HD) [1]. The changes 

in lipid metabolism may affect the disease progression or 

pathogenic mechanism. Amyloidogenic peptide is believed to 

play a key role in the AD pathogenesis mounting the evidence 

that dyslipidemia provoke the production or reduce of amyloid 

beta (Aβ) clearance [2]. Moreover, other dyslipidemic-related 

conditions have also been linked in the AD pathogenesis, 

including obesity, hypertension, inflammation, insulin 

resistance, and type 2 diabetes [3]. In this review, we focus on 

the lipid and cholesterol metabolism, with an overview of the 

various lipid and cholesterol metabolic pathways and changes 

that have been linked to AD.  

Cholesterol and Lipid Metabolism  

Rising evidence suggest the changes in the metabolism of 

lipids, predominantly cholesterol, is implicated directly in the 

pathogenesis of many neurodegenerative disease including AD 

[2]. This part describes the cholesterol synthesis and 

metabolism followed by some vital information about the lipid 

transport and metabolism, in order to explain the normal roles 

of these lipids in the body and the brain. Some changes in lipid 

metabolisms which have been detected in AD [4].  

Cholesterol Synthesis and Metabolism 

Cholesterol plays a vital function in the structure and function 

of cell membranes. It influences the inflexibility of lipid 

bilayers, there in affects the transfer and process through the 

membrane. Cholesterol in the brain accounts for 25% of the 

total body cholesterol [5]. About 70% of its cholesterol is there 

in the myelin, 20% is present in the glial cells, while the 

remaining 10% is present in the neurons [6]. The cholesterol 

requirements in the body are met by dietary intake of animal 

fats, or by synthesis. Cholesterol productiongets activated when 

acetyl-CoA is transformed into 3-hydroxy-3methylglutaryl-

CoA (HMG-CoA). Cholesterol is formed when its precursor 

lanosterol is channeled into either the Bloch pathway to 

generate desmosterol or lathosterol respectively; these are then 

converted to cholesterol [7].  

Cholesterol is used widely in the body, particularly by the 

cell membrane structures. Other important physiological 

functions include the production of bile by the liver and 

hormone synthesis. Brain cholesterol metabolism is different 

and independent from that of peripheral tissues, due to the 

blood–brain barrier (BBB) preventing rapid transport into and 

out of the brain [8]. In the adult brain, cholesteroloriginate in the 

form of non-esterifies form, rest being in the form of 

desmosterol and cholesteryl esters [9]. Major part of cholesterol 

(about 70–80%) is seen in the myelin sheaths formed by 

D 

mailto:suji648@yahoo.co.in


Sujeetha & Anand                                                                                                                   Cholesterol and Alzheimer’s  

  

Vol 1 | Issue 1 | Apr – Jun 2022                                                                                     Indian J Pharm Drug Studies | 11  

oligodendrocyte that insulates the axons and in the plasma 

membranes of astrocytes and neurons, where it maintains 

cellular morphology, plays important roles in lipid rafts, and 

helps in the synaptic transmission [10]. During adolescence, the 

cholesterol turnover reduces because of myelin sheath 

formation with the half-life between six months and five years. 

This is a contrast turnover that occurs during the general circulation 

[6].  

The role of lipid rafts in neurodegenerative diseases  

Lipid rafts are buoyant membrane glycolipoprotein micro 

domains rich in cholesterol and sphingolipids [11]. These 

provide the frame for signaling molecules and protein 

transduction, trafficking and immunoglobulin functions and 

neurotransmitters [12]. Lipid rafts have been linked to various 

diseases conditions including cardiovascular disease and certain 

cancers. They are also important for the entry, replication, 

assembly, and budding of various types of viruses [13]. Some 

proteins are linked with lipid rafts include GPI-anchored 

proteins, Src family kinases, components of the heterotrimeric 

G-proteins and many of the proteins linked to AD linked with 

the metabolism of APP [14]. Some of the later include the γ-

secretase complex (processes over 20 proteins, including γ-site 

cleavage of APP), BACE-1 (β-site APP cleaving enzyme, the 

enzyme responsible for βsite APP cleavage), ADAM10 (A 

Disintegrin and Metalloprotease-10, enzyme which cleaves 

APP at the α-site, also cleaves TNF-α and E-cadherin), and 

neprilysin, an Aβ-degrading enzyme [15]. Studies have 

demonstrated that by increasing the dietary cholesterol content, 

Aβ production can be elevated [16].  

In animal studies where rabbits were placed on a high-

cholesterol diet, a greater level of brain Aβ accumulation was 

found [17]. Lim et al., [18] concluded that a high-fat and  high-

cholesterol (HFHC) diet results in increase in brain cholesterol 

esters, These effects were seen in  older APO E E4 knock-in 

mice compared to APO E E3 mice. Conversely, the reduction of 

cell membrane cholesterol has been shown to reduce γ-secretase 

activity and also to increase the non-amyloidogenic α-secretase 

cleavage of APP [19, 20]. Studies have shown that the 

membranes of the lipid content raft, from early-stage AD brain 

frontal and entorhinal cortex tissue, has greater microviscosity 

which correlated with BACE-1/APP interaction levels [21]. 

This was found not to be due to increased cholesterol or 

sphingomyelin levels, but due to a lower content of unsaturated 

fats [14]. This adds to the evidence that dyslipidaemia is central 

in AD neurodegeneration and that a diet high in polyunsaturated 

fatty acids may provide benefit in slowing or preventing AD 

pathogenesis. Transgenic AD mouse models and mathematical 

modeling studies support this theory, with evidence suggesting 

that increasing the cholesterol and long-chain polyunsaturated 

fatty acid (mainly DHA) content of membranes may delay the 

onset and/or progression of AD [22]  

Alzheimer’s disease  

AD is the most common type of dementia, characterized by the 

progressive loss of memory and other cognitive functions of the 

brain. An affected individual gradually becomes totally 

dependent upon others, culminating in their death 

approximately 3– 10 years after diagnosis [23]. The 

neurodegenerative changes that are characteristic of an AD 

brain include widespread synaptic and neuronal loss, the 

accumulation of extracellular Aβ fibrils and plaques, 

intracellular neurofibrillary tangles (NFT) composed of hyper-

phosphorylated tau filaments, microglial infiltration, and brain 

atrophy, particularly in the regions important for memory, such 

as the hippocampus, amygdala, and frontal cortex [24]. Genetic 

mutations in genes whose proteins are involved in the 

processing of the APP to Aβ peptides, such PS1 and PS2, as 

well as AD-related APP mutations, are predisposing risk factors 

for AD. However, these mutations are involved only in 

earlyonset familial Alzheimer’s disease (EOAD) which occurs 

before age 65, but sometimes as young as 30. These cases are 

relatively rare and account for less than 5% of all AD cases [25].  

The main risk factor linked to the much more common 

late-onset form of Alzheimer’s disease (LOAD) is APOE E4 

allele status. Other significant risk factors include dyslipidemia, 

hypertension, obesity, chronic inflammation, insulin resistance, 

and type 2 diabetes. All of these are also risk factors for 

cardiovascular disease. When these conditions occur together, 

this is termed ‘metabolic syndrome’ [28, 29]. It is believed that 

metabolic changes caused by these conditions lead to a greater 

production or reduced clearance (or both) of Aβ peptides. Many 

of these risk factors can be prevented by altering diet and 

physical exercise, which are known to reduce the risk of 

cardiovascular disease. There is a growing body of evidence 

that reducing these same risk factors would considerably slow 

or possibly prevent AD pathogenesis [30, 31].  

Effect of Amyloid-Β on Lipid Metabolism  

It has been suggested that APP processing affects cellular lipid 

metabolism [32]. In cultured neurons and in transgenic mice, 

Aβ with 42 amino acids (Aβ42) can activate neutral 

sphingomyelinases and down regulate sphingomyelin levels, 

whereas Aβ40 reduces de novo cholesterol synthesis by 

inhibiting the activity of HMG-CoA reductase. Therefore, 

maintaining lipid homeostasis could be a biological function of 

APP processing Grimm et al., [33] and the pathological 

accumulation of Aβ could lead to abnormal lipid metabolism. 

Furthermore, both studies in vitro and in AD patients suggest 

that Aβ causes oxidative stress, leading to lipid oxidation that 

might contribute directly to neurodegeneration [32] Studies also 

suggest that Aβ induces ozonolysis of cholesterol, leading to the 

formation of peroxiderivatives that accelerate aggregation of 

Aβ monomers [35] and that Aβ oxidizes cholesterol at positions 

of 7-β and 3-β, thus leading to H2O2 production [36]. Therefore, 



Sujeetha & Anand                                                                                                                   Cholesterol and Alzheimer’s  

  

Vol 1 | Issue 1 | Apr – Jun 2022                                                                                     Indian J Pharm Drug Studies | 12  

a deleterious feedback loop between Aβ accumulation and 

altered lipid metabolism could be one of the molecular 

mechanisms underlying the link between lipid disorders and 

AD.  

Cholesterol metabolism-related genes and Alzheimer’s 

disease  

APO E protein plays a central role in lipid transport while 

possession of the APOE E 4 allele influences AD risk. The 

human APOE gene is located on chromosome 19, and its three 

most common alleles are designated E2, E3 and E4(Williams et 

al., 2020). Of these, E3 is the most common allele in humans 

(78%) followed by E4 (14%), then E2 (8%). However, it is 

usually APO E E4 which is associated with increased levels of 

circulating LDL cholesterol, higher triglyceride levels, and a 

greater risk of coronary artery disease (Linton et al., 2019). This 

is despite APO E E4 having higher affinity for the LDL 

receptors than APO E E3 and E2, and increased levels of 

lipoprotein internalization [37, 38].The increased affinity of 

APO E E4 for the LDL receptor in the periphery may be a 

limiting factor for cellular processing of lipoproteins, for it has 

been observed that APO E E4 is poorly recycled by cells, yet is 

readily internalized which results in raised intracellular 

cholesterol levels [39].  

APO E in the brain  

Whilst APO E is clearly a molecule of great importance in the 

CNS, it is not imported from the periphery [40] where the liver 

produces it in the largest amounts. Rather it is synthesized 

locally by astrocytes in significant quantities [41]. LRP-1 is 

primarily expressed in neurons, whereas glial cells mostly 

express the LDL-receptor [42]. These receptors (particularly 

LRP-1) are not only used for lipoprotein metabolism, but they 

also bind some proteins involved in brain development (e.g. 

Sonic Hedgehog, Wnt, and reelin), as well as proteases, 

protease inhibitors, vitamin transporters, and proinflammatory 

molecules [43]. Receptor-mediated endocytosis transit lipid 

particles to late endosomes.  Immediately after endocytosis, 

APO E is detached from the lipid components and is not sent to 

lysosomes but recycled back to the plasma membrane [44].   

APOE 4 and Alzheimer’s disease  

One of the strongest genetic risk factors for AD risk is APOE 

E4 allele, the mechanisms is still implicit. A study that 

examined the physical distribution of the resultant APOE E4 

protein shows that it gravitates towards the larger, less dense 

particles of CNS lipoprotein whereas APOE E2 and APOE E3 

tend to associate with smaller, denser lipoprotein fractions [45]. 

Like their peripheral counterparts, the CNS APOE proteins 

have differential effects, where APOE E2 and APOE E3 appear 

to be more effective than APOE E4 [46]. Early studies showed 

that plasma levels of APOE may be an important factor in AD, 

as higher levels were observed in the plasma of AD individuals 

relative to non-AD individuals [47, 48]. Other early studies 

suggested that polymorphisms in the APOE promoter region 

may influence the probability of developing AD [49, 50].  

This region, which belongs to the TATA box family, 

regulates the production of APOE protein where a genotype of 

-491TT produces much less APOE than -491AT and -491AA. 

The initial studies demonstrated that the APOE -491AT and AA 

genotypes lead to increased risk for AD independent of APOE 

allele [51]. It was soon realized that the risk for AD may be 

compounded when APOE E4 alleles and the 491 AA genotype 

are combined [42]. These results suggested that the improved 

production of the APOE protein may boost disease progression 

but did not account for any mechanism of action in AD by the 

APOE E4 protein itself. However, more recent studies now 

suggest that low plasma APOE levels increase the risk of AD 

[53]. Furthermore, Baker-Nigh et al., 2016 concluded that the 

levels of AAPO E and CNS are not correlated but it is well 

correlates CSF Aβ levels which are more relevant to AD risk. 

CONCLUSION 

Reducing the risk of AD will involve dietary changes and 

healthy lifestyles that can reduce the risk of dyslipidaemia, 

insulin resistance, type 2 diabetes, cardiovascular disease, and 

chronic inflammation, which are all known risk factors for AD. 

Despite the many studies on the influence of the APOE E4 allele 

on Aβ aggregation, binding, and clearance, the overall 

pathological effect of this allele is still not known. It is hoped 

this will pave the way towards effective treatments, whilst 

highlighting the importance of preventing dyslipidaemia.  

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Vol 1 | Issue 1 | Apr – Jun 2022                                                                                     Indian J Pharm Drug Studies | 14  

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190(35):E1033-41. 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

How to cite this article: Sujeetha Purushothaman, 

Arumugan Vijaya Anand. The Link between Cholesterol 

and a Brain Disease. Indian J Pharm Drug Studies. 2022; 

1(1): 10-14. 

Funding: None;                 Conflict of Interest: None Stated  

 


