ALZHEIMERS DISEASE

PRESENTED BYASHISH AFZAL AKHIL AKSHAY XYZ ANJALI

ALZHEIMERS DISEASE AN INTRODUCTION

NOMENCLATURE OF AD

Alzheimers disease has been named after the German psychiatrist ALOIS ALZHEIMER, who first described this disease in 1901 in Auguste D, a fiftyyear-old woman.

ALZHEIMERS DISEASE (AD)

AD

is an irreversible, progressive brain disease that slowly destroys memory and thinking skills. A chronic, irreversible, terminal, progressive, neurodegenerative brain disorder characterized by progressive dementia It usually affects older individuals & is the most common cause of dementia among people with age 65 years & more.

ALZHEIMERS DISEASE (AD)

NEURODEGENERATIVE DISEASES are the disorders characterized by progressive loss of CNS neurons & their processes. DEMENTIA refers to a progressive, irreversible decline in mental function, impairment of memory, intellect & personality.

Classification of AD
Depending on its time of onset AD may be : Early-onset AD (presenile AD) It is rare, usually affecting people aged 30 to 60 years & usually running in families. Late-onset AD (senile AD) It is comparatively more common. It usually affects people over age 65 yrs.

ALZHEIMERS DISEASE (AD)

ETIOLOGY OR FACTORS CAUSING AD

FACTORS CAUSIND AD
Although, the exact cause of AD is not known, but few risk factors are as follows NON MODIFIABLE RISK FACTORS : Aging Environmental Female gender Genetics MODIFIABLE RISK FACTORS : Diabetes Hypertension Metabolic syndrome Head injury

FACTORS CAUSIND AD
AGE : The risk of developing AD increases with age. AD is not a part of normal aging. It is caused by fatal disease that affects brain. Acc. To Alzheimers Association, 10% of all people over the age of 65 have AD 50% of all people over the age of 85 have AD

FACTORS CAUSIND AD
GENDER: AD affects woman more frequently than men. FAMILY FACTORS: A clear, inherited pattern of AD exists for approx. 10% of all cases. DOWN SYNDROME: people with DS often develop Alzheimer dis. In their 30s & 40s,although the exact reason is not known. ENVIRONMENTAL AGENTS: especially viruses & aluminum toxicity are also the possibilities

ALZHEIMERS DISEASE (AD)

SYMPTONS & STAGES

SYMPTONS & STAGES

STAGE 1

Mild memory loss

STAGE 2

Worsening of intellectual functions, Personality changes, Speech & language problem

STAGE 3

Patients depend on others for activities of daily living viz. eating, dressing, bathing.

SYMPTONS & STAGES

Stage 1: Early stage Decreased judgment, Inability to perform mathematical cal, Inability to understand imaginary things. Stage 2: Middle stage Changes in usual habits, seizure, depression,hallucinogens,delusion,involuntary urination Stage 3:Severe dementia Unable to remember how to talk, toilet, swallow, eventually become bedridden,immobility,develops pneumonia,dehydration

ALZHEIMERS DISEASE (AD)

PATHOLOGICAL CHANGES IN AD

PATHOGENESIS
Depending on the primary cause pathogenesis of the AD can be explained by following 3 major hypothesis Neurotransmitter(cholinergic) hypothesis Amyloid hypothesis Tau hypothesis

HYPOTHESIS

NEUROTRANSMITTER HYPOTH. Suggest that AD is initiated due to: reduced synth.of Ach, which in turn is due to reduced activity of choline acetyl transferase Redn in no. of cholinergic neuron. Levels of other neurotransmitters viz. serotonin,norepinephrine,somatostatin are also reduced. AMYLOID HYPOTHESIS: Accumulation & abnormal production of beta Amyloid peptides initiates neuron degeneration as obs. In AD.

HYPOTHESIS

Beta Amyloid is, short peptide, is abnormal proteolytic byproduct of transmembrane protein Amyloid Precursor Protein (APP). TAU HYPOTHESIS suggest that neurons have internal support structure partly made up of microtubules. A protein called tau stabilizes microtubules. In AD, TAU undergoes unusual chemical changes & gets hyperphosporylated & causing microtubules to collapse. tau protein clumps together to form Neurofibrillary Tangles.

ALZHEIMERS DISEASE (AD)

PHARMACOTHERAPY

CLASSIFICATION
Cholinergic activators (anticholinesterase): Tacrine Rivastigmine, granistigmine Donepezil, galantamine. Glutamate antagonist : Memantine Nootropic: Piracetam New drug : Huperzine-A Miscellaneous : Pyritinol, ginkgo biloba Nicergoline, piribedil.

MECHANISM OF ACTION
Increasing global cerebral blood flow Direct support of neuronal metabolism.. Enhancement of neurotransmission. Improvement of discrete cerebral function. Activation of neuronal metabolism. Antioxidant action.

DRUGS (MARKETED PREP) ARICEPT Used to delay or slow the symptoms of

(Donepezil) AD Loses its effect over time Used for mild, moderate and severe AD Does not prevent or cure AD Used to reduce depression and anxiety May take 4 to 6 weeks to work Sometimes used to help people get to sleep Used to treat severe aggression Also used to treat depression and anxiety

CELEXA (Citalopram)

DEPAKOTE (Sodium Valproate)

EXELON (Rivastigmine)

Used to delay or slow the symptoms of AD Loses its effect over time Used for mild to moderate AD Can get in pill form or as a skin patch Does not prevent or cure AD

NAMENDA
(Memantine

Used to delay or slow the symptoms of AD Loses its effect over time Used for moderate to severe AD Sometimes given with Aricept, Does not prevent or cure AD
Used to prevent or slow the symptoms of AD Loses its effect over time Used for mild to moderate AD Does not prevent or cure AD Used to reduce depression & anxiety May take 4 to 6 weeks to work Sometimes used to help people get to sleep Used to treat severe aggression Also used to treat depression and anxiety

RAZADYNE
(Galantamine )

ZOLOFT
(Sertraline )

TRILEPTAL
(Oxcarbazepine)