Ayurvedic medicine is a personalized system of traditional medicine native
to India and the Indian subcontinent. It is based on a holistic view of
treatment which promotes and supports equilibrium in different aspects of
human life: the body, mind, and soul. Popular Ayurvedic medicinal plants
and formulations that are used to slow down brain aging and enhance memory
include

 Ashwagandha* (Withania somnifera)*, Turmeric* (Curcuma longa)*,
Brahmi* (Bacopa
monnieri)*, Shankhpushpi (*Convolvulus pluricaulis, Evolvulus alsinoides*,
and other species), gotu kola* (Centella asiatica)*, and guggulu (*Commiphora
mukul* and related species) and a formulation known as Brāhmī Gh*ṛ*ita,
containing Brahmi, Vacā* (Acorus calamus)*, Ku*ṣṭ*ha* (Saussurea lappa)*,
Shankhpushpi, and Purāṇa Gh*ṛ*ita (old clarified butter/old ghee).

    The rationale for the utilization of Ayurvedic medicinal plants has
depended mostly on traditional usage, with little scientific data on signal
transduction processes, efficacy, and safety. However, in recent years,
pharmacological and toxicological studies have begun to be published and
receive attention from scientists for verification of their claimed
pharmacological and therapeutic effects.

Ayurvedic medicine for prevention and treatment of dementia.

1. Introduction      Due to an increase in life expectancy, it is estimated
that the number of elderly people worldwide will increase to approximately
2.1 billion by the year 2050 (Indian Govt survey) . Increase in age is a
major risk factor for dementia, a clinical neurodegenerative syndrome
characterized by impaired memory and activities of daily living, altered
behaviour, personality, and other cognitive dysfunctions (Figure 1
<https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5976976/figure/fig1/>).
Several types of dementia have been reported in human patients, including
Alzheimer type of dementia (AD), vascular dementia, Lewy body dementia, and
dementia as a result of diseases such as stroke, AIDS, and multiple
sclerosis. Among these, AD is the most common cause of dementia and is
characterized by progressive memory loss and other cognitive deficits,
including impaired judgment and decision-making, and language disturbances.
In contrast, vascular dementia is defined as loss of cognitive function
resulting from ischemic, hyperperfused, or haemorrhagic brain lesions.
Major risk factors for dementia include old age, long-term consumption
of “western”
diet, physical and cognitive inactivity, and epigenetic and environmental
factors. Other risk factors for dementia include cardiovascular and
cerebrovascular problems, excessive alcohol consumption, social isolation,
traumatic brain injury, and having one or two copies of the APOE*ϵ*4
genetic variant.

<https://www.ncbi.nlm.nih.gov/core/lw/2.0/html/tileshop_pmc/tileshop_pmc_inline.html?title=Click%20on%20image%20to%20zoom&p=PMC3&id=5976976_ECAM2018-2481076.001.jpg>

<https://www.ncbi.nlm.nih.gov/core/lw/2.0/html/tileshop_pmc/tileshop_pmc_inline.html?title=Click%20on%20image%20to%20zoom&p=PMC3&id=5976976_ECAM2018-2481076.001.jpg>

Figure 1 <https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5976976/figure/fig1/>

Symptoms of dementia.

Ayurvedic medicine is a personalized system of traditional medicine native
to India and the Indian subcontinent. It is based on a holistic view of
treatment which promotes and supports equilibrium in different aspects of
human life: the body, mind, and soul. Ayurveda dates back to the period of
the Indus Valley civilization (about 3000 B.C.) and has been passed down
through generations of oral tradition, like the other four knowledge texts
(vedas) in ancient India. These include the Rigveda, Yajurveda, Samaveda,
and Atharvaveda, which were composed between the 12th and 7th century B.C.
Ayurvedic medicine includes descriptions of over 5000 signs and symptoms of
various diseases and 700 herbs and 6,000 formulations to treat them. A
direct reference to dementia in Ayurvedic literature has not been
mentioned. However, the symptoms of forgetfulness and memory loss have been
described. Ayurvedic medicine mentions and explains the use of several
herbs and their qualities for the treatment of nervous system disorders,
including memory loss typically seen in older adults, but only recently
have mechanistic studies been carried out, to determine the effects of
these herbs on CNS disorders such as AD. In recent years, there is renewed
interest in the use of phytochemicals for the treatment of dementia, since
pharmacological treatment of dementia using drugs (haloperidol,
risperidone, aripiprazole, olanzapine, cholinesterase inhibitors,
memantine, and benzodiazepines) is often inadequate and has many side
effects.

2. Ayurvedic Medicinal Plants for the Treatment of Dementia

The use of complementary medicines, such as plant extracts, in dementia
therapy varies according to different cultural traditions. Ayurvedic
medicinal herbs modulate the neuro-endocrine-immune systems and are also
rich sources of antioxidants and anti-inflammatory compounds. They are
claimed to enhance memory and rejuvenate cognitive functions. Several
Ayurvedic medicines have been exploited for the treatment and management of
acute and chronic neurological diseases. Examples of popular Ayurvedic
medications include Brāhmī Gh*ṛ*ita, Divya Medha Kwath, and Brento Forte.
These formulations induce specific effects on brain functions, such as
increase in blood flow and maintenance of memory.

2.1. Ashwagandha

Ashwagandha (*Withania somnifera*, fam. Solanaceae), or Indian Ginseng, is
a common herb used in Ayurvedic medicine as an adaptogen or antistress
agent. Ashwagandha root contains a large variety of compounds including 12
alkaloids, 40 withanolide, and several sitoindosides and flavonoids.
Withaferin A (WL-A) and withanolide A are two constituents which show
similar pharmacokinetic profiles, except that the oral bioavailability for
WL-A is 1.44 times greater than that of withanolide A. These components
produce antistress, antioxidant, and immunomodulatory effects in acute
models of experimental stress. According to Ayurvedic medicine, Ashwagandha
constituents provide a number of healthful effects such as youthful state
of physical and mental health and increase in happiness. It is not only
given to children as tonics but is consumed by the middle-aged and elderly
to increase longevity. Recent studies have indicated that Ashwagandha root
improves the body's defense against chronic diseases not only by improving
cell-mediated immunity, but also through producing potent antioxidant and
anti-inflammatory effects that protect against cellular damage caused by
free radicals and inflammatory mediators. At the molecular level,
Ashwagandha root may produce beneficial effects in AD by inhibiting the
activation of NF-*κ*B, blocking *β*-amyloid (A*β*) production, reducing
apoptotic cell death, restoring synaptic function, and enhancing
antioxidant effects through the migration of Nrf2 to the nucleus, where it
increases the expression of antioxidant enzymes. It is suggested that WL-A
activates the translocation of Nrf2 to the nucleus, where the transcription
factor upregulates the expression of neuroprotective proteins, such as
hemeoxygenase-1. Treatment of human neuroblastoma SK-N-SH cells with
methanolic extracts of Ashwagandha root results in dendrite extension,
neurite outgrowth, and synapse formation. Moreover, treatment of cultured
rat cortical neurons with A*β* (25–35) (10 *μ*M) produces axonal and
dendritic atrophy and pre- and postsynaptic loss, and these changes were
abrogated by treatment with WL-A (1 *μ*M). WL-A also attenuates the
expression of semaphoring 3A to facilitate neural regeneration. The
beneficial effects of Ashwagandha root constituents in neurodegenerative
diseases may be due to their neurite promoting, antioxidant,
anti-inflammatory, antiapoptotic, and anxiolytic activities, as well as
their ability to improve mitochondrial dysfunction and restore energy
levels and increase levels of antioxidant defenses such as reduced
glutathione.. It should not be taken with barbiturate-type sedatives, since
the herb can increase the effectiveness of these drugs. Ashwagandha can
cross the blood-brain barrier and lower inflammation in the brain.

2.2. Turmeric   Curcumin (C21H20O6) or diferuloylmethane (bis-*α*,*β*
-unsaturated *β*-diketone) is a hydrophobic polyphenolic compound (mol mass
of 368.38) present in turmeric (an ingredient in curry powder). It is
derived from the rhizome of* Curcuma longa*, which belongs to the family
Zingiberaceae. It has antioxidant, anti-inflammatory, and cancer chemo
preventive properties. Curcumin reduces oxidative damage and improves
cognitive functions related to the aging process. It induces antioxidant
effects by modulating the Nrf2-keap1 pathway and reduces genomic
instability events. Nrf2 is primarily present in the cytoplasm, where it is
bound with the Kelch-like ECH-associated protein 1 (Keap1). Interaction of
curcumin with Keap 1 releases Nrf2, which migrates into the nucleus and
binds as a heterodimer to antioxidant responsive elements in DNA, to
initiate target gene expression. Nrf2-regulated genes include antioxidant
enzymes, molecular chaperones, DNA repair enzymes, and anti-inflammatory
response proteins. These proteins promote the reduction in ROS generation
while increasing the ability of the cell to repair any subsequent damage.
Curcumin also suppresses proinflammatory pathways by blocking the
production of TNF-*α*, IL-1*β*, and other proinflammatory cytokines,
including IL-8, MIP-1*β*, and MCP-1, in astrocytes and microglia. Curcumin
attenuates neuroinflammation through the inhibition of phospholipase A2 (PLA
2) and cyclooxygenase (COX-2) enzymes associated with the metabolism of
neural membrane phospholipids to prostaglandins. It reduces glial
fibrillary acidic protein (GFAP) expression, improves spatial memory in the
A*β*-induced rat model of AD, and decreases GFAP and COX-2 expression in A
*β*-treated astrocytes. Both* in vitro* and* in vivo* studies indicate that
curcumin binds with A*β* and inhibits its aggregation, as well as fibril
and oligomer formation.* In vivo* studies have shown that dietary curcumin
not only crosses the blood-brain barrier and decreases A*β* deposition in
AD transgenic mice, but also markedly inhibits Tau phosphorylation. The
absorption rate and bioavailability of curcumin can be increased by
consuming it with black pepper* (Piper nigrum)*. Studies have indicated
that piperine, an active ingredient in black pepper, increases the
bioavailability and bioefficacy of curcumin by inhibiting its
glucuronidation. Interestingly, consumption of piperine and curcumin has
been found to protect against chronic unpredictable stress-induced
cognitive impairment and oxidative damage.

2.3. Brahmi* (Bacopa monnieri)    Bacopa monnieri* belongs to the family
Scrophulariaceae and is found throughout the Indian subcontinent in wet,
damp, and marshy areas. It has many branches with small oblong leaves and
purple flowers. This plant is not only used for the treatment of a number
of nervous system disorders such as insomnia, anxiety, and epilepsy, but
also used for enhancing memory and the intellect [55
<https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5976976/#B55>]. In Ayurvedic
medicine,* Bacopa monnieri* is used as a memory enhancing,
anti-inflammatory, analgesic, antipyretic, sedative, and antiepileptic
agent, which acts as a nootropic (repairing damaged neurons and improving
brain function). According to Ayurvedic medical practitioners, the memory
enhancing properties of* Bacopa monnieri* are due to the presence of
bacoside A, assigned as 3-(a-l-arabinopyranosyl)-O-*β*-d-glucopyranoside-10,
20-dihydroxy-16-keto-dammar-24-ene, and bacoside B

2.4. Shankhpushpi     Shankhpushpi* (Convolvulus pluricaulis)* is a common
plant in India. It belongs to the family Convolvulaceae. The whole plant of
Shankhpushpi is used in various formulae as a nervine tonic for improvement
of memory and cognitive function. Shankhpushpi is recommended for nervous
system disorders, such as stress, anxiety, mental fatigue, and insomnia. It
has been suggested that Shankhpushpi has a calming effect by regulating the
body's production of the stress hormones, adrenaline and cortisol. The
major bioactive components of* Convolvulus pluricaulis* are glycosides,
flavonoids, coumarins, anthocyanins, and alkaloids. Sitosterol glycoside,
octacosanol tetracosane, hydroxycinnamic acid, and glucose have also been
isolated from the plant. These metabolites contribute to its nootropic and
memory enhancing properties, along with its other pharmacological
activities. Ethanolic extracts of Shankhpushpi improve learning and memory
and induce antioxidant effects in rats. Furthermore, ethanolic extracts of
the whole Shankhpushpi plant, when administered to cholesterol-fed gerbils,
induce reduction in serum levels of cholesterol, LDL cholesterol,
triglycerides, and phospholipids. The administration of ethanolic extracts
of Shankhpushpi increases acetylcholine content in fields CA1 and CA3 of
the hippocampus in a dose-dependent manner. This is accompanied by a
significant increase in the number of dendritic intersections, branch
points, and dendritic processes arising from the cell bodies of neurons, in
comparison with age-matched saline controls. Results suggest that ethanolic
extracts of Shankhpushpi enhance memory by increasing neurite outgrowth.

2.5. Gotu kola    Gotu kola* (Centella asiatica)* is another herb that is
known as Brahmi (besides* Bacopa monnieri*). It belongs to the family
Apiaceae and is a perennial creeping herb with long thick stems and smooth
fan leaves. It is widely used as a blood purifier and for treating high
blood pressure, enhancing memory, and promoting longevity. Tea made from
gotu kola can be very helpful for relieving tension, relaxing the mind, and
soothing anxiety. As a nervine adaptogen, constituents of gotu kola are
capable of increasing intelligence, longevity, and memory. In the Ayurvedic
system of medicine, water extracts of gotu kola are used not only for
rejuvenating and restoring neural cells, but also for stimulating healthy
sleep. It has a powerful effect on quality of life in disorders such as
epilepsy. The primary active ingredients of gotu kola are saponins (also
called triterpenoids), which include asiaticosides, in which a
trisaccharide moiety is linked to the aglycone asiatic acid, madecassoside,
and madasiatic acid. Other components isolated from* Centella asiatica* such
as brahmoside and brahminoside may be responsible for CNS and uterorelaxant
actions but have yet to be confirmed by clinical studies. At the molecular
level, asiaticoside derivatives from gotu kola (asiatic acid and
asiaticoside) are capable of reducing hydrogen peroxide-induced cell death,
decreasing free radical levels, and inhibiting A*β*-mediated neural cell
death* in vitro*. Results suggest a role for gotu kola in the prevention
and treatment of A*β* toxicity and AD type of dementia. Gotu kola extracts
possess antioxidant activity and can alter mitochondrial function. Because
mitochondrial dysfunction is a common process that contributes to
neurodegeneration in many neurodegenerative diseases, there are potentially
broad implications for the use of water extracts of gotu kola.

2.6. Guggulu    Guggulu is an oleogum resin exuding from cracks and
fissures or incisions in the bark of several plant species including*
Commiphora
mukul, Commiphora molmol, Commiphora abyssinica, Commiphora Burseraceae*,
and* Commiphora wightii*. It is pale yellow or brown in color with an
aromatic odor and bitter astringent taste. Guggulu preparations contain 30%
to 60% water-soluble gum, 20% to 40% alcohol-soluble resins, and about 8%
volatile oils, which have many biological activities. Water-soluble
extracts of guggulu contain mucilage, sugars, and proteins. Alcohol-soluble
extracts of guggulu contain commiphoric acids, commiphorinic acid, and
heerabomyrrhols. The volatile constituents of guggulu include terpenes,
sesquiterpenoids, cuminic aldehyde, eugenol, the ketone steroids Z- and
E-guggulsterone, and guggulsterols I, II, and III. Guggulu contains ferulic
acids, phenols, and other nonphenolic aromatic acids which are potent
scavengers of superoxide radicals and can be important for the treatment of
neurodegenerative diseases that are associated with oxidative stress. In
addition, guggulsterones antagonize nuclear hormone receptors and decrease
cholesterol levels, which may explain the hypolipidemic effects of guggulu
extracts. Many studies have indicated that there is a link between
cholesterol, amyloid precursor protein processing, and AD. Cholesterol is
an essential modulator of the physicochemical state and functional activity
of the cell membrane and thus plays an essential role in the regulation of
synaptic function and neuronal plasticity.* In vitro* and* in vivo* modulation
of membrane cholesterol levels affect different cholesterol pools within
the plasma membrane bilayer that are differentially sensitive to the
disrupting effect of A*β*. It is likely that beneficial effects of guggulu
on AD may be due to its cholesterol-lowering effects. Decreased neuronal
cholesterol levels, in turn, inhibit the A*β*-forming amyloidogenic
pathway, possibly by removing amyloid precursor protein from cholesterol
and sphingolipid-enriched membrane microdomains. These intriguing
relationships raise hopes that cholesterol-lowering strategies may
influence the progression of dementia associated with AD. Administration of
guggulipid (Z-guggulsterone) significantly lowers both serum LDL
cholesterol and triglyceride levels, supporting the view that guggulipids
may produce beneficial effects in the cardiovascular system.

3. Conclusion    Popular Ayurvedic medicinal plants (Ashwagandha, Turmeric,
Brahmi, Shankhpushpi, gotu kola, and guggulu) not only reduce brain aging
and induce antistress and memory enhancing effects which help in
regeneration of neural tissues, but also induce antioxidant,
anti-inflammatory, antiamyloidogenic, nutritional, and immune-supportive
effects in the human body. Scientific validation and the documentation of
Ayurvedic medicines are essential for their quality evaluation and global
acceptance. Therapeutic efficacy of Ayurvedic herbal formulations might be
enhanced, not only by achieving purity, but also through a better
understanding of their biological effects. These days attempts are underway
to achieve this goal. Once it is done, large multicenter clinical trials of
Ayurvedic medicine can be planned and performed in patients with dementia
and other neurodegenerative disorders.

Conflicts of Interest     The authors declare that there are no conflicts
of interest regarding the publication of this paper.

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 KR  IRS  4223

On Sat, 4 Feb 2023 at 09:08, 'venkat giri' via iyer123 <
[email protected]> wrote:

> *Respected Sir/s,*
>
> *     DEMEMTIA ......*a serious mental problem caused by brain disease or
> injury, that affects the ability to think, remember and behave normally.
> மூளைநோய் காரணமாக அல்லது மூளையில் அடிபடுதலால் உண்டாவதும் சிந்திக்கும்
> திறன், நினைவாற்றல், இயல்பான நடத்தை ஆகியவற்றைப் பாதிப்பதுமான கடுமையான மனநலக்
> கேடு.
> Alzheimer's disease is the most common cause of dementia.
> அல்சைமர் என்பது மூளையை பாதிக்கும் ஒரு வகை மூளை நோயாகும். இந்த நோய்
> முதியவர்களிடயே பொதுவானதாகும். இந்த நோயால் பாதிக்கப்பட்டவர்களின் ஞாபக
> சக்தி குறைகிறது மற்றும் மிகவும் பலவீனமான நினைவகத்தை கொண்டுள்ளனர். மேலும்,
> அவர்களின் மூளை சரியாக செயல்படுவதில்லை. இதன் காரணமாக அவர்களின் அன்றாட
> நடைமுறை படிப்படியாக மோசமடையத் தொடங்குகிறது. அல்சைமர் என்பது ஒரு வகை
> டிமென்ஷியா ஆகும், இதனை முழுமையாக குணப்படுத்த இயலாது
>             The absence of effective treatments for dementia underscores
> the importance of strategies, including maintaining a healthy lifestyle, to
> attenuate the risk factors for dementia.
> Studies have shown that higher physical activity levels and lower
> sedentary behaviours could reduce the risk of dementia. However, such
> studies have generally relied on self-reports with limited accuracy.
>                            A recent study using accelerometers to
> accurately measure physical activity levels showed that
> moderate-to-vigorous physical activity and daily steps, but not light
> physical activity and sitting, were associated with a lower risk of
> cognitive decline in older women.
>                            A study published in the journal Alzheimer’s &
> Dementia shows that higher levels of moderate-to-vigorous physical activity
> and daily steps were associated with a lower risk of mild cognitive
> impairment (MCI) and dementia in women aged 63  yrs and older. In
> addition, the study found that moderate-to-vigorous intensity steps, but
> not light-intensity steps, were associated with a lower risk of cognitive
> decline. This study helps to clarify the intensity of physical activity
> needed to prevent or delay cognitive decline.
> *                         Dr. Raphael Wald, Psy.D., a neuropsychologist
> says: “*This is a way of further confirming what we already knew while
> stressing the importance of moderate to vigorous exercise.* The study
> also shows that there is no real cap on the cognitive gains that can be had
> from physical activity. The more you can safely do more it decreases one's
> risk for cognitive decline.”*
>               *The study found that including 31 minutes of additional
> daily moderate-to-vigorous physical activity was associated with a
> reduction in the risk of MCI or dementia by 21%. Similarly, including an
> additional 1,865 steps in the daily routine was associated with a 33% lower
> risk of cognitive decline.*
>
>                   Evidence suggests that women are at a greater risk of
> dementia than men. For instance, one study found that the lifetime risk of
> dementia was 20% in women and 10% in men aged 45 years.
>                    Given the elevated risk of dementia in women, the study
> used hip accelerometers to assess whether there is a link between physical
> activity, sedentary behavior, and the risk of cognitive decline and
> dementia.
> Impact of daily steps and physical activity.
> *                                                      A **long-term** study
> that consisted of 1,277 women with an average age of 82 yrs , aimed at
> preventing chronic conditions in postmenopausal women. The participants
> included in the study did not have symptoms of MCI or dementia at the onset
> of the study. *
>           The researchers used hip accelerometers to measure the levels of
> low intensity and moderate-to-vigorous physical activity, as well as
> sedentary behaviour. They were also able to differentiate between
> light-intensity and moderate-to-vigorous-intensity steps using the
> accelerometer.
>                          Researchers monitored the participants over an
> average follow-up of 4.2 years, during which 267 individuals were diagnosed
> with mild cognitive impairment or probable dementia. Higher levels of
> moderate-to-vigorous physical activity and daily steps were associated with
> a lower risk of MCI and dementia.
>
>
> BENEFITS OF ENHANCED DAILY ACTIVITY
>
>                        The participants with moderate-to-vigorous physical
> activity in the highest quartile, i.e., the group of individuals who
> engaged in higher levels of moderate-to-vigorous physical activity than 75%
> of the remaining participants, performed an average of at least 61 minutes
> of moderate-to-vigorous physical activity daily. In contrast, the lowest
> quartile, i.e., the bottom 25%, consisted of women who engaged in less than
> 23 minutes/day of moderate-to-vigorous physical activity.
> The participants with moderate-to-vigorous physical activity levels in the
> highest quartile were at a 36% lower risk of MCI than those in the lowest
> quartile. The difference in dementia risk was not statistically
> significant. However, participants in the highest quartile of daily steps
> (at least 4050 steps/day) were at a 64% lower risk of mild cognitive
> impairment and 52% lower risk of dementia symptoms than women in the lowest
> quartile (less than 1867 steps).
>
>
> What are the causes of Alzheimer's disease?
>
>          Mostly, people above the age of eighty-five are affected by
> Alzheimer's disease.
> Head trauma can also cause Alzheimer's disease. Also, Alzheimer's disease
> causes sleep disorders.
> This disease is also caused by genetics.
>
> Symptoms of Alzheimer's disease are:
>
>    - Memory loss, which is usually noticed by someone else.
>    - Difficulty communicating or finding words.
>    - Difficulty with visual and spatial abilities, such as getting lost
>    while driving.
>    - Difficulty reasoning or problem-solving.
>    - Difficulty handling complex tasks.
>    - Difficulty with planning and organizing.
>    - Difficulty with coordination and motor functions
>    - Confusion and disorientation
>
> *Thes lead to the following **psychological **changes.*
>
>    1. Personality changes
>    2. Depression
>    3. Anxiety
>    4. Inappropriate behaviour
>    5. Paranoia...*a type of mental illness in which you wrongly believe
>    that other people want to harm you.**மற்றவர்கள் தனக்குத் தீங்கு செய்ய
>    விரும்புவதாகத் தவறான முறையில் நம்புகிற மன நோய் வகை.*
>    6. Agitation
>    7. Hallucinations... a false perception of objects or events involving
>    our senses: sight, sound, smell, touch and taste. Hallucinations seem real,
>    but they're not. Chemical reactions and/or abnormalities in brain cause
>    hallucinations.
>
>
> *PREVENTION:*
> *                There's no sure way to prevent dementia, but there are
> steps one can take that might help. *
>
> *!. Keep mind active.... Mentally stimulating activities, such as reading,
> solving puzzles and playing word games, and memory training might delay the
> onset of dementia and decrease its effects.*
> *Be physically and socially active. Physical activity and social
> interaction might delay the onset of dementia and reduce its symptoms. Aim
> for 150 minutes of exercise a week.*
> *2.Quit smoking. Some studies have shown that smoking in middle age and
> beyond might increase risk of dementia and blood vessel conditions.
> Quitting smoking might reduce risk and will improve health.*
> 3.Take enough *vitamins...* *Some research suggests that people with low
> levels of vitamin D in their blood are more likely to develop Alzheimer's
> disease and other forms of dementia. One can get vitamin D through certain
> foods, supplements and sun exposure.*
> *4. **Manage cardiovascular risk factors. Treat high blood pressure, high
> cholesterol and diabetes. Lose weight if overweight.*
> *5.**High blood pressure might lead to a higher risk of some types of
> dementia. *
> *6.Maintain a healthy diet. A **diet —** rich in fruits, vegetables,
> whole grains and omega-3 fatty acids.*
> *7.** Good-quality sleep.   Practice good sleep **hygiene.*
> *Treat hearing problems. People with hearing loss have a greater chance of
> developing cognitive decline. Early treatment of hearing loss, such as use
> of hearing aids, might help decrease the risk.*
>
> *By 2050, 11.44 million people in India are expected to be living with
> dementia, which is up from 3.84 million in 2019, according to the Global
> Burden of Disease study.*
>      Worldwide
> *, at least 44 million people are living with dementia, making the disease
> a global health crisis,necessiating   to be addressed vehemently.*
> *-------*
> *Regards*
> *V.Sridharan*
> *Trichy*
>
>
>
>
>
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